Break The Silence

Kasus HIV/AIDS pada Ibu Rumah Tangga Terus Meningkat

2011-05-30T17:22:00.000-07:00

http://health.kompas.com/index.php/read/2011/05/31/06031498/Kasus.HIVAIDS.pada.Ibu.Rumah.Tangga.Terus.Meningkat
Lusia Kus Anna | Selasa, 31 Mei 2011 | 06:03 WIB

Merauke, Kompas - Pengidap HIV/AIDS di kalangan ibu rumah tangga di Merauke, Provinsi Papua, terus meningkat. Bulan Januari hingga April 2011, dari 33 kasus baru pengidap HIV/AIDS, 10 di antaranya ibu rumah tangga.

Sekretaris Komisi Penanggulangan HIV/AIDS (KPA) Merauke Henny Astuti Suparman, Senin (30/5), menuturkan bahwa risiko tertinggi tertular kini tidak lagi pada kelompok pekerja seks, tetapi beralih ke kelompok ibu rumah tangga. ”Sumber penularan dari hubungan seksual,” kata Henny di Merauke.

Berdasarkan data KPA Merauke, jumlah pengidap HIV/AIDS di Merauke hingga bulan Maret 2011 ada 1.283 orang. Dari jumlah tersebut, 630 laki-laki dan 607 perempuan. Sisanya tidak diketahui.

Dari jumlah tersebut, 196 orang adalah pekerja seks, 168 petani, dan 165 (12,86 persen) ibu rumah tangga. Jumlah ibu rumah tangga pengidap HIV/AIDS meningkat dibandingkan dengan data bulan Desember 2010 sebanyak 158 orang (12,57 persen).

”Bulan April 2011, kami temukan lagi tiga ibu rumah tangga positif HIV/AIDS,” kata Henny.

Menurut dia, 3 dari 10 ibu rumah tangga pengidap HIV/AIDS tahun 2011 sedang hamil. Diduga mereka tertular dari suami. ”Setelah diperiksa, ternyata suaminya positif. Namun ada juga suami tak mau dites,” katanya.

Ironisnya, ada ibu hamil yang positif HIV/AIDS tak mau mendapat pengobatan antiretroviral (ARV). ”Dia merasa sehat dan baik-baik saja sehingga merasa tidak butuh ARV ataupun pendampingan,” kata Henny.

Di Kabupaten Asmat, penyebaran HIV/AIDS juga cepat. Pada tahun 2006 tercatat satu orang terinfeksi. Sementara tahun 2010 ditemukan ada 41 orang yang terinfeksi. (RWN)

HIV/AIDS Infections Jump Sharply in Papua

2011-05-21T03:33:00.000-07:00

http://www.aidsindonesia.or.id/hivaids-infections-jump-sharply-in-papua-the-jakarta-globe.html
The Jakarta Globe

Jayapura. The number of people living with HIV/AIDS in Papua and West Papua has jumped by more than 30 percent to over 17,000 in just four months, an official said on Thursday.

Kostan Karma, head of the Papua AIDS Prevention Commission (KPA), said the spike in infections was very worrying, and blamed it on the prevalence of unprotected sex.

He said the latest data from the provincial health office showed there were 7,098 people with the virus in Papua in December, and 10,000 in West Papua. “But back in August 2010, there were only 5,000 in Papua and 8,000 in West Papua,” he said.

“ The KPA is trying hard to campaign about HIV/AIDS prevention, but we just can’t seem to keep the numbers down.”

Kostan said that of the 38 towns and districts in the two provinces, Mimika in Papua, home to the world’s biggest copper and gold mine, had shown the highest increase and overall number of infections. However, he did not give any figures.

The KPA also blamed the proliferation of new districts over the past 10 years as a factor for the spread of the virus.

“What’s happened is that there’s been more money spreading around, which encourages people to break with the traditional way of life and adopt a more modern lifestyle, including sexual promiscuity,” Kostan said.

“What we’re trying to do is get churches to spread the message to get people to stop having casual sex, or if they must, to at least use a condom.”

He said that if the number of people living with the virus rose to 1 percent of the population of both provinces — which the 2010 census put at 2.8 million — the KPA would begin imposing mandatory testing for all new mothers in the region.

He said the measure would at least help identify the number of infected newborns, so they could get early treatment.

Inilah 'Obat Super' Penakluk HIV & Malaria

2011-05-12T05:02:00.000-07:00

http://teknologi.inilah.com/read/detail/1503892/inilah-obat-super-penakluk-hiv-malaria

Oleh: Billy A Banggawan

Teknologi - Kamis, 12 Mei 2011 | 09:47 WIB

INILAH.COM, Jakarta – Virus penyebab AIDS, HIV, membunuh dua juta manusia tiap tahun di dunia. Parasit yang disebarkan nyamuk, malaria, menginfeksi 225 juta manusia dan membunuh 781 ribu tiap tahun.

Penyakit-penyakit ini menyerang manusia sejak pertama kali menyebar ke manusia dari monyet 40 tahun lalu. Di kemudian hari, penyakit-penyakit ini menjadi musuh bebuyutan manusia dan tubuh manusia telah berevolusi untuk memeranginya.

Kedua pembunuh ini, baru dan lama, sebenarnya memiliki molekul yang sama. Karena hal ini, satu ‘obat super’ akan bisa melawan penyakit-penyakit tersebut. Obat itu adalah, HIV Protease Inhibitor (HIV PI). Obat ini dirancang khusus ilmuwan untuk mengobati HIV dengan mencegah virus mematikan itu membangun proteinnya dengan benar.

“HIV PI saat ini sedang digunakan secara klinis dan merupakan obat HIV terkemuka,” kata Kepala Laboratorium Parasitologi Kedokteran Photini Sinnis di Langone NYU Medical Center. Obat ini telah mengubah wajah pengobatan HIV beberapa tahun terakhir. Orang yang mengonsumsi obat ini tak lagi mati karena AIDS.

Protease merupakan enzim-enzim yang bisa memotong protein menjadi bentuk yang benar, hal ini memungkinkannya menjadi aktif. HIV PI menghentikan virus HIV di treknya dengan cara mencegah salah satu enzim protease melakukan pekerjaannya.

Tanpa kerja protease, protein HIV tak akan terpotong dan tidak aktif. Alhasil, unit HIV yang disebut virion tak dapat mengumpulkannya untuk membuat virion baru. Tubuh manusia memiliki mekanisme alami membunuh virion HIV untuk mencegah virus mereplikasi diri pada tingkat yang tak dapat ditangani tubuh.

Selama beberapa tahun terakhir, beberapa kelompok penelitian (termasuk kelompok Sinnis) telah menyadari efek samping positif yang mengejutkan dari HIV PI spesifik. “Kami menemukan, obat ini memiliki sifat anti-malaria,” kata Sinnis.

Para peneliti yakin, HIV PI menghentikan munculnya protease dalam parasit malaria seperti yang mereka lakukan pada protease HIV. Kelompok Sinnis menemukan, obat anti-HIV ini mencegah parasit bereplikasi pada tikus.

Belum ada percobaan pada manusia namun hasil awal pada tikus membuat peneliti HIV menganjurkan penggunaan eksklusif PI untuk pengobatan HIV di Afrika. “Di Afrika, HIV dan malaria banyak yang tumpang tindih, obat-obatan HIV yang digunakan harus PI,” kata Sinnis.

Setelah itu, obat ini akan memberi manfaat tambahan pada infeksi malaria yang ada, yakni dengan menghambatnya. Saat ini, PI hanya berguna untuk memerangi malaria pada orang yang memiliki HIV. PI lebih beracun dibanding banyak obat yang digunakan untuk memerangi malaria itu sendiri.

Namun, jika PI dapat disesuaikan menjadi kurang beracun, obat ini bisa menjadi obat tunggal malaria. Ketika hal itu terjadi, obat ini akan menjadi senjata. Pasalnya, malaria sendiri dengan cepat mengembangkan kekebalan pada obat anti-malaria yang ada, jadi obat baru selalu sangat dibutuhkan.

Meski begitu, untuk mengembangkan obat anti-malaria yang bisa berdiri sendiri didasarkan pada obat anti-HIV, protease spesifik dalam malaria yang menjadi target HIV PI pertama harus ditemukan. “Jika kita bisa menemukan target protease, kita bisa merancang obat yang lebih baik dan tentunya tanpa racun,” kata Sinnis.

Sejauh ini, ilmuwan telah mempersempit kelas protease yang mungkin mengandung protease target namun mereka belum menemukan satu protease spesifik. Namun, sebuah makalah di Journal of the Federation of American Societies for Experimental Biology (FASEB), Colin Berry dan rekan di Cardiff University di Wales menemukan protease yang dihambat HIV PI dalam parasit Leishmania, kerabat malaria.

Meski protease yang disebut Ddi 1 ini belum diidentifikasi dalam malaria, kelompok Berry dan yakin protease inilah yang dicari-cari. “Hasil penelitian kami menunjukkan, protein Ddi1 merupaka target HIV (PI), dan menunjukkan Ddi1 Leishmania sebagai target potensial terapi antiparasit,” Berry.

“Melalui identifikasi protein ini, kami berharap bisa mengeksploitasi kelemahan parasit ini untuk mengembangkan terapi baru yang efektif memerangi penyakit-penyakit yang berbahaya,” lanjutnya.

Menurut Sinnis, makalah Berry memberi harapan dan ide-ide dalam menemukan target parasit malaria. Ketika ditemukan, obat anti-HIV sekaligus anti-malaria dapat dikerjakan. [mdr]

Ditemukan, Antibodi Mampu Lawan Virus HIV

2011-05-12T04:55:00.000-07:00

http://www.mediaindonesia.com/mediahidupsehat/index.php/read/2011/05/11/4042/9/Ditemukan-Antibodi-Mampu-Lawan-Virus-HIV
Rabu, 11 Mei 2011 16:00 WIB

Penulis : Prita Daneswarim

PENELITIAN terbaru yang digelar Universitas Melbourne berhasil mengungkap imunitas terhadap HIV. Mereka kemudian mengembangkan vaksin untuk membangun antibodi melawan virus tersebut.

Dengan menganalisis peran antibodi manusia bernama ADCC pada pasien HIV, peneliti mampu mengidentifikasi keterlibatan virus dengan antibodi.

Profesor Stephen Kent dan salah seorang koleganya menyebutkan, "Antibodi ADCC memiliki implikasi kuat dalam perlindungan terhadap HIV dalam beberapa uji coba vaksin, tapi peran mereka memang belum dipahami secara pasti."

"Hasil penelitian ini menunjukkan virus HIV sangatlah mudah berpindah tempat, tapi terbukti pula antibodi ADCC mampu mencegah virus tersebut berkembang lebih cepat dan membuatnya lebih lemah," kata Kent.

Tampak pula, antibodi ADCC yang bagus bisa benar-benar digunakan untuk melawan infeksi melalui vaksin dan menghentikannya. Hasil penelitian ini telah diterbitkan pada jurnal PNAS edisi Mei 2011.(Pri) (Pri/OL-06)

Kisah Nyata dan Fakta Tentang HIV-AIDS di Indonesia, Menghitung Hari

2009-12-01T01:36:00.000-08:00

http://ruanghati.com/2009/11/30/kisah-nyata-dan-fakta-tentang-hiv-aids-di-indonesia-menghitung-hari/

2009 November 30

by ruanghatiberbagi

Dalam sebuah rumah berdinding semen dan berkamar tiga di Sorong, Papua Barat, impian Angelina pun perlahan memudar. Dulu ia pernah bercita-cita untuk menjadi seorang polisi wanita “karena saya melihat mereka membantu dan melindungi orang.”

Namun sudah lama impian itu sirna. Pada Juni 2002, suaminya yang bekerja sebagai ahli mekanik meninggal. Enam bulan kemudian bayi perempuan pertamanya pun juga meninggal. Baru pada bulan Oktober ia tahu penyebabnya. Belum juga hilang kesedihannya, perempuan 21 tahun itu diberitahu bahwa ia terinfeksi HIV. Kemungkinan besar suaminya terjangkit virus itu dari pekerja seks.

Angelina hanya salah satu korban yang polos dan tidak tahu menahu tentang HIV di Indonesia. Ia hanya orang biasa yang bahkan tidak pernah melakukan tindakan beresiko tetapi tertular oleh orang yang berkelakuan tidak baik. Tentu saja banyak perhatian tercurah pada penyebaran HIV/AIDS di antara kelompok-kelompok yang beresiko. Tapi UNICEF justru memfokuskan pada anak muda dalam upayanya mencegah penularan virus ke masyarakat luas.

Sebagian besar anak muda Indonesia tidak tahu mengenai HIV/AIDS dan penyebarannya. Hanya sedikit yang mendapat informasi yang tepat tentang penyakit itu. Dalam satu penelitian, hanya satu dari tiga pelajar sekolah menengah atas di Jakarta yang tahu persis cara pencegahan penularan virus secara seksual.

Penderita AIDS yang sudah tinggal menghitung hari, nikmat sesaat namun akibatnya sangat mengenaskan

Kurangnya pengetahuan ini menjadi sebuah bom waktu di daerah-daerah seperti Papua. Di sana anak muda mulai aktif secara seksual pada awal masa pubertas. Dengan memberikan pelatihan pada guru-guru sekolah menengah atas di Papua tentang ketrampilan hidup dan HIV/AIDS, UNICEF berharap generasi muda di Papua akan memahami konsekuensi dari seks yang tidak aman.

Menyangkut pendidikan sebagai satu pilar strategi lima tahun HIV/AIDS, pemerintah Indonesia tetap berjalan di tempat. Karena itu UNICEF mencoba langkah berbeda dengan menyentuh langsung pelajar sekolah menengah atas.

“Saat kita berada di sekolah, kita mengkombinasikan strategi pendidikan ketrampilan hidup dan pendidikan sebaya untuk mencegah penularan HIV dan penyalahgunaan obat-obatan. Strategi itu pada dasarnya dirancang untuk memberikan kaum muda ketrampilan komunikasi antar pribadi, kreatifitas, kepercayaan diri, harga diri dan daya pikir kritis. Ini perlu untuk membantu mereka jika menghadapi kesempatan untuk mencoba obat-obatan atau melakukan seks yang tidak aman,” kata Rachel Odede, kepala unit HIV/AIDS UNICEF Indonesia.

Hambatan utama untuk pendidikan orang Indonesia adalah keyakinan bahwa penyakit ini hanya menjangkiti “orang tidak baik” dan memang mereka layak mendapatkannya. Orang yang terinfeksi HIV/AIDS pun diberi stigma dan dipaksa pergi dari kampung halaman mereka. Mereka ditolak berobat ke dokter, diancam, dijauhi dan disingkirkan. Ketakutan dan stigma semacam itulah yang membuat para tetangga dan bahkan anggota keluarga Angelina tidak tahu sama sekali penyakitnya.

“Saya anggota aktif di gereja. Saya tidak ingin orang melihat ke saya dan berkata ‘Lihat, orang itu putrinya sakit’”, kata Yakobus, ayahnya. Ia seorang guru sekolah dasar yang mengambil pensiun dini untuk merawat putri bungsunya itu.

Meski orang Indonesia yang sekuler telah mengenal program keluarga berencana dengan slogan ‘dua anak cukup’, pembicaraan mengenai seks masih dianggap tabu oleh sebagian penduduk yang sebagian besar Muslim dan konservatif ini. Saat ini epidemi HIV/AIDS terkonsentrasi pada tingkat penularan HIV yang masih rendah pada penduduk secara umum. Namun pada populasi tertentu, tingkat penularannya cukup tinggi, yaitu di antara para pekerja seks komersil dan pengguna jarum suntik yang kian meningkat.
Seperti halnya Vietnam dan China, epidemi HIV/AIDS di Indonesia masih digolongkan baru timbul. Para pakar memperkirakan ada sekitar 90.000 sampai 130.000 orang Indonesia yang terjangkit HIV. Tapi UNICEF yakin angka ini akan bertambah jika tidak ada perubahan perilaku populasi yang beresiko dan menjadi perantara.

Tidak sulit melihat gambaran penularan ini di masyarakat umum. Diperkirakan ada 7 sampai 10 juta laki-laki Indonesia mengunjungi pelacuran tiap tahunnya. Mereka biasanya enggan menggunakan kondom. Diperkirakan juga ribuan perempuan telah terinfeksi secara seksual oleh laki-laki yang menyuntikkan obat-obatan.

“Pada tahun-tahun setelah krisis moneter, kami melihat makin banyak orang muda pergi ke kota untuk mencari pekerjaan. Tampak pula terjadi peningkatan jumlah pekerja seks dan pengguna jarum suntik (IDU),” kata Dr Barakbah, kepala unit penyakit menular Rumah Sakit Dr Soetomo, Surabaya. “Kita akan melihat lonjakan kasus AIDS dalam beberapa tahun mendatang. Kita juga melihat pertumbuhan eksponensial pada kasus-kasus HIV yang dilaporkan, terutama yang berasal dari tempat pelacuran. Penyebarannya sedang memasuki tahap ketiga, yang mengarah ke AIDS. Kami melihat makin banyak pasien,” tambahnya.

Untuk mengetahui bagaimana skenario ini terkuak, lihatlah kisah pekerja seks berusia 16 tahun, Reena (bukan nama sebenarnya). Ia beroperasi di Surabaya, daerah seks terbesar di Asia. Ia terinfeksi HIV positif dan ia tidak tahu. Ia pun tetap melayani tamunya sampai 12 orang tiap minggunya. Tak satupun para pelanggannya dan beberapa ‘pacarnya’ itu yang menggunakan kondom.

Orang-orang tersebut adalah di antara 2.000 lebih pelaut yang singgah setiap minggunya di Surabaya, ibu kota Jawa Timur yang juga pusat pengiriman barang antara Jawa, Sulawesi, dan kepulauan bagian timur Indonesia.

Orang dari seluruh penjuru Nusantara menjuluki Surabaya dengan istilah ‘tiga M’ dalam kaitannya dengan penularan HIV/AIDS, yaitu “Men (laki-laki), Money (uang ) dan Mobility (mobilitas)”.

Saat ini instansi-instansi makin menaruh perhatian terhadap cepatnya penularan HIV/AIDS terhadap generasi muda Indonesia yang menggunakan jarum suntik. Sebagian besar dari mereka berumur dua puluhan dan aktif secara seksual.

Di beberapa daerah di Jakarta, diperkirakan 90 persen pengguna terkena HIV positif. Beberapa tahun lalu, demografi para pengguna obat-obatan mulai meningkat karena jatuhnya harga heroin dan para ahli kimia Indonesia mulai membuat shabu-shabu dalam jumlah besar (bahkan cukup untuk menjadi eksporter obat bius).

Seperti halnya di Thailand, penggunaan obat-obatan menarik para orang miskin di kota di Indonesia. Merekalah kelompok yang sulit diberi pengertian mengenai jarum suntik pribadi dan bersih.

Untuk mendorong kaum muda untuk memanfaatkan layanan pengujian dan konseling, UNICEF memberi dukungan teknis dan finansial kepada beberapa lembaga swadaya masyarakat untuk membantu generasi muda putus sekolah yang rentan terhadap penyalahgunaan obat dan eksploitasi seks.

Tapi lembaga-lembaga ini tidak bisa berjuang sendirian. Untuk memberi pemahaman ke masyarakat yang lebih luas, mereka butuh dukungan dan sumber-sumber dari pemerintah pusat dan daerah. Sayangnya, instansi pemerintah enggan untuk memimpin gerakan ini karena penyakit itu dianggap sebagai akibat dari ‘tindakan amoral’.

Beberapa langkah baru telah diambil. Para gubernur dari daerah-daerah yang penularannya parah bersedia menandatangani perjanjian dan bersumpah untuk memusatkan segala sumber mereka untuk kemajuan penyuluhan mengenai penyakit itu. Tapi rupanya masih terlalu banyak hal yang harus dikerjakan.

“Tantangan terdekat yang saya lihat adalah menterjemahkan strategi HIV/AIDS menjadi rencana tindak yang operasional dan konkrit,” kata Odede. (Unicef)

Deadly Denial - Confronting AIDS in Asia

2008-03-30T21:16:00.000-07:00

http://www.un.org/Pubs/chronicle/2008/webarticles/080327_aids.html

By United Nations Secretary-General Ban Ki-Moon

As a Korean, and the first UN Secretary-General from Asia in more than 30 years, it’s no surprise that I often speak of my home continent as a model for economic development. Yet when it comes to the AIDS epidemic, I am more disheartened than proud.

Across Asia, AIDS remains the most likely cause of death of people in their most productive years. At the rate we are going, the current 5 million Asians infected with HIV will grow to 13 million by 2020. Meanwhile the death toll mounts, with some 440,000 people succumbing to AIDS each year.

Asia’s flourishing economic prosperity does not help groups that are most vulnerable to the disease. People living with HIV—including many in low-risk groups—are denied their basic right to health.

This is deplorable, considering how little is required to contain the epidemic and help those in need. A new UN-supported survey, “Redefining AIDS in Asia: Crafting an effective response,” finds that annual investment of just thirty cents per capita can reverse the epidemic through prevention. That would translate into saving the lives of more than 200,000 people each year.

Special event to remember 25 years of AIDS, at UN Headquarters in New York. (Photo: UN Photo/ Mark Garten)

I know my continent has the resources, the technology and the ability to undertake this ambitious and life-saving mission. Asia’s fast-growing economies have emancipated millions of poor people. Most countries on the continent are on track to achieve the Millennium Development Goals, our common vision for building a better world in the 21st century.

But if we fail to act, we could threaten the very prosperity that places Asia in a position to respond effectively now. We are in danger of spinning into a vicious circle where the AIDS epidemic grows so serious as to undermine economic growth and social resilience, leading to more and more infections at ever greater cost.

Experience shows Asia’s ability to act in the face of grave threats. We saw this in the response to SARS five years ago. Beyond the immeasurable good of saving lives, action will bring a tangible economic boost. For every dollar we spend on preventing HIV today, the report notes, we will save eight dollars on treatment in the future.

Our response to AIDS is not only about money. It is, above all, about people. The stigma associated with AIDS can be worse than the disease – robbing people of access to basic human rights and health care, preventing them from living a dignified life, and deterring them from getting tested for HIV.

Some of my most inspiring experiences as Secretary-General have been my meetings with UN+, the group of our staff members living with HIV. Their courage and expertise have given me new and invaluable insights into the epidemic. Hearing from these people, who speak with such directness about their lives, I felt ashamed of the discrimination that people living with HIV often face around the world, and perhaps especially in Asia. Painful as these lessons may be, I value them and intend, on my next visit, to visit a facility or organization addressing the needs of those living with HIV and AIDS.

Listening is important. But beyond that we must engage with people living with HIV as we develop policies and carry out programmes to address the epidemic.

Women and girls are the main caregivers – and they are also disproportionately vulnerable to HIV infection. They need special attention. We must tackle social norms that prevent women from protecting themselves, including through better legislation, or better enforcement of existing laws.

And we must guard against legislation that blocks universal access by criminalizing the lifestyles of vulnerable groups. We have to find ways to reach out to sex workers, men who have sex with men and drug users, ensuring that they have what they need to protect themselves.

It starts with Asian Governments showing leadership to invest more substantially in the fight against AIDS and move resolutely to stamp out stigma and discrimination.

This June, the UN General Assembly will hold a high-level meeting offering an opportunity to take stock and advance the global response to AIDS. I personally will do all I can – as a Secretary-General and an Asian – to be at the vanguard of this effort. I look to the leaders of Asia to do the same.

HIV/AIDS Management Programme

2008-02-26T21:05:00.000-08:00

http://lifesenseonline.co.za/?page_id=18

LifeSense’s HIV/AIDS Management Programmes are orientated to changing employees’ attitudes towards HIV/AIDS. The goal of the programmes is one of engaging and providing awareness as well as treatment for employees. It is with such requirements for support to employees, that LifeSense has developed its comprehensive HIV/AIDS Management
Programme utilizing the 4 “A’s”, namely:

HIV/AIDS AWARENESS CAMPAIGNS
The objective of the campaigns is to raise awareness of HIV/AIDS in all areas and divisions within a company. This is achieved by the campaign utilising various forms of activities, such as:-

Presentations
Workshops
Plays / Theatre Productions
Pamphlets and Posters
Talks

VOLUNTARY, COUNSELING AND TESTING (VCT)
LifeSense utilises both its own as well as local medical staff to perform VCT. The company’s size, national distribution as well as the industry it operates in, is taken into account when determining the most efficient and cost effective strategy for performing VCT to all employees and not just members of medical schemes. The VCT service includes:

Pre-test counseling
An HIV/AIDS test
Post-test counseling

PERSONAL PROTECTION PROGRAMME (P3)
The increasing rate of HIV/AIDS infections in South Africa has necessitated the need for an infection prevention programme. The P3 programme provides assistance for employees who have suffered a possible accidental exposure to HIV/AIDS as a result of rape, needlestick, motor vehicle accident, assault and sport injuries etc. The programme protocols are based upon the employee having just 72 hours to combat the risk of HIV/AIDS infection. The benefits include access to:

24 hour, 365 days Care Centre for advice and counseling
Two medical consultations and blood tests
Starter pack of 3 days ART’s
Combination ART treatment for a further 28 days
Additional benefits for sexual exposure

HIV / AIDS DISEASE MANAGEMENT
LifeSense has the expertise to manage employees living with HIV/AIDS and employ professional healthcare staff to ensure effective HIV/AIDS disease management for these employees.
The following steps form part of the HIV/AIDS Disease Management Programme that employees living with HIV/AIDS will access to:-

Application to enrol on the management programme
Follow-up of enrolled members
Confidentiality
Progress reports
Treatment protocols

DELIVERABLES
LifeSense’s HIV/AIDS Management Programmes are pro-active and a highly effective step against HIV/AIDS, as they assist companies to minimize the risk that HIV/AIDS presents. When viewed against the R1.8 to R2.2 billion annual absenteeism cost to companies in South Africa associated to HIV/AIDS alone, these programmes provide an element of ontrol for employers over their employees when it comes to HIV/AIDS.

MANAGING HIV

2008-02-26T20:10:00.000-08:00

http://www.managinghiv.com/home_managinghiv.asp

Managing HIV is dedicated to providing high-quality information to people with the human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS). Thanks to advances in diagnosis and treatment, more and more people are living with HIV and AIDS. Managing HIV offers these individuals—and their friends and family—a broad range of information on AIDS and HIV. Managing HIV covers HIV symptoms and the latest AIDs and HIV medications and provides expert advice on when to start treatment and coping with treatment side effects. All of this information is available in video, audio and text formats. Whether you're looking for a health professional to clearly explain a new therapy or people who are living with HIV and AIDS to share their experiences, Managing HIV is your online resource.

HIV & AIDS Statistics

- Approximately 40,000 new HIV infections occur each year in the U.S.
- Approximately 50 percent of adults living with HIV are women
- The CDC estimate that up to 950,000 U.S. residents are living with HIV
- Approx. 5 million new HIV infections occurred worldwide during 2002
- Early HIV symptoms often include, swelling of the lymph nodes, headache, fever, loss of appetite, sweating, and sore throat

HIV Basics

The Grim Reaper: Club Drugs And HIV

Many people think that the HIV epidemic is over. But recently there has been a spike in the number of new infections. Experts say that certain club drugs that allow for wild uninhibited sex are to blame.
Watch Video >> Read Transcript >>

The Grim Reaper:

Club Drugs And HIV

Participants: Perry N. Halkitis, PhD Assistant Professor and Chair of Applied Psychology, New York University School of Medicine

Webcast Transcript

ANNOUNCER: Thanks to advances in HIV treatments people in the US who have good access to healthcare are living longer healthier lives. But experts are now seeing a worrisome trend.

PERRY HALKITIS, PhD: Infection rates were stable during the 1990s, but, in the last few years, there's been a spike in new HIV transmissions across the population and especially among gay and bisexual men.

ANNOUNCER: Explaining this turnaround is not so simple.

PERRY HALKITIS, PhD: First of all, there's a fatigue around HIV that we're seeing in the gay population and in the general population. People feel that the HIV epidemic is over, they're more complacent about safer sex practices, they think there's a cure and, as a result, people are not being as safe or as responsible in their sexual behavior.

So number two, I think what's happening is that prevention efforts really haven't evolved and haven't become as sophisticated as people have become sophisticated around HIV. So "Use a condom every time" campaigns, which worked fine in the early 1980s and the mid-1980s are no longer effective.

What we're also seeing is this complex interaction that exists between sexual risk-taking and drug use. And in particular with a subset of drugs known as "club drugs."

ANNOUNCER: And if hearing the term "club drugs" conjures up images of a disco ball or a rave you'd be mistaken.

PERRY HALKITIS, PhD: Our research shows very clearly that people do them at home, they do it with their friends, they do it in the park, they do it wherever they need to do it.

ANNOUNCER: So what are the so called "club drugs?"

PERRY HALKITIS, PhD: You know, twenty years ago, we would have been talking about cocaine as the primary drug, but that doesn't seem to be the big problem. It is a problem, but not the biggest problem these days.

We're talking about methamphetamine, also known colloquially as "crystal." We're talking about MDMA, which is known commonly as "ecstasy." We're talking about ketamine and we're talking about Rohypnol and we're still talking about cocaine, to some extent. And we're talking about, more importantly, not just each of these drugs in isolation, but each of these drugs being used often in combination with each other, in combination with alcohol, in combination with prescription drugs such as Viagra.

ANNOUNCER: And that, say experts, is a menacing mixture.

PERRY HALKITIS, PhD: Perhaps the most worrisome is methamphetamine crystal. This is a psychostimulant, it's a form of speed; it's related to ecstasy. It's related to other amphetamines and it has been a huge problem.

Crystal is a hypersexual drug. It's a hugely disinhibiting drug, so that we know, and it's been clearly documented, that people who are using this substance have sex without rational thinking, they have multiple partnerings; they just let go. They feel like they're on top of the world, so nothing is a problem and any rational thinking, any logical thinking around safer sex practices completely gets wiped away.

Do they realize after they come down from their high that they've had unsafe sex? Yes, they do. Can they do anything about that? No, it's too late.

ANNOUNCER: And as users try to keep the high going, they move from snorting to smoking and eventually to injecting.

PERRY HALKITIS, PhD: We not only have a drug in which people's inhibitions are erased, basically, around safer sex, but now men, women, whoever are using these substances, whoever is using meth is injecting. And so transmission through injection and the sharing of needles and the sharing of works creates another route of HIV transmission that is linked to methamphetamine use.

ANNOUNCER: And using crystal can have severe consequences for HIV positive people taking lifesaving antiretroviral medications.

PERRY HALKITIS, PhD: What we know, from our work, is that adherence, taking your medications the way you're supposed to take them, is a problem across the board. And if we believe the literature, people are supposed to be adherent 95 percent of the time. Very hard for people to be adherent 95 percent of the time when they're high. When they're feeling good, the last thing they want to do is actually stop to remember to take their medications.

Number two, we know that methamphetamine is an immunosuppressant. Methamphetamine that is sold on the street is not pure methamphetamine. It's been cut with talc; it's been cut with heroin; it's been cut with a variety of other substances. That has an effect on people's immune systems.

Number three and probably most alarming of all is some recent studies that came out that indicate, even if an individual is highly adherent to his or her medications, even if. If they're using methamphetamine, replication of the virus in the brain is accelerated.

ANNOUNCER: So whether you're a man, woman, gay or straight you are walking on dangerous ground when you mix drugs with sex.

PERRY HALKITIS, PhD: To people who haven't started who hear wonderful tales about this drug: Don't. This is not a wonderful drug. The price that you will pay in the long run is not worth it. To people who are started, I say, look for help. Because what do we know about methamphetamine and its affects on people's lives? There's enormous social deterioration. People become physically ill and they become socially ill. They lose their friends, they lose their family and they lose their jobs.

I think, as a society, we need to step up to the plate with HIV. Men, women, young adults who are becoming sexually active need to realize that the HIV epidemic is not over.

Spermicides and Condoms: Not the Best Marriage?

It is a well-known fact that consistent and correct use of condoms can prevent pregnancy. But condoms are not perfect. They've been known to break on occasion, and people don't always use them correctly. That's why doctors have recommended that they be used in conjunction with an over-the-counter spermicide for extra birth-control insurance.
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Spermicides and Condoms: Not the Best Marriage?

By Peggy Crane

But say the word "condom" and what comes to mind more often is its reputation as the method of choice for practicing safe sex. Condoms are now primarily used to prevent many sexually transmitted diseases, including HIV, the virus that causes AIDS.

In the late 1980s, nonoxynol-9, a product that has been on the market for more than 50 years and is the main ingredient in most spermicides, began to show promise as a method for preventing HIV transmission when it was observed to kill the virus in a test tube. The public and the medical community alike hailed N-9 as the newest HIV preventative, and many condom manufacturers hastened to lubricate their products with the chemical.

Unfortunately, hopes were dashed when more recent studies — including a four-year World Health Organization study of HIV-negative female sex workers in Africa and Thailand — showed N-9 to be ineffective in the prevention of HIV infection. In fact, researchers discovered that when used frequently, products containing N-9 may even increase the risk of acquiring the virus.

Understanding what N-9 can and cannot do can be daunting, much less making the right choices regarding its use. Below, Rowena Johnston, Ph.D., Associate Director of Basic Research at the American Foundation for AIDS Research (amfAR), shares the latest findings about N-9 and stresses correct condom use as still the best defense against HIV transmission for men and women alike.

Are condoms a foolproof method of HIV prevention?
If everybody used them all the time, condoms would do a good job of slowing down transmission. The problem is that people don't use condoms all the time. People often feel uncomfortable insisting on the use of a condom with their partner. We really need products that don't require a partner's consent. That way, we'd feel free to protect ourselves and take charge of our own health.

Many people think they are at low risk for HIV, so why take the trouble to use a condom?
Some women may think of themselves as fairly low-risk and therefore might not insist on the use of condoms. But that's a serious mistake. There are straight men out there, too, who don't think they need to protect themselves from infection because they still think HIV is a "gay" disease.

Why don't people use condoms more consistently when this simple device is obviously the key to safe sex?
I think what we're seeing now is kind of a fatigue. People have been aware that they should be practicing safe sex since the 1980s. Our sense is that people are kind of getting sick of being good all the time. You know, it's as if you're on a diet and sometimes you want to eat chocolate. But that's precisely why you should stick with the diet.

How does Nonoxynol-9 work against HIV?
HIV is a virus that has a fatty membrane around it, just like our own cells have. Nonoxynol-9 is essentially a detergent. Detergents cut through grease, and that's exactly how N-9 kills HIV and other sexually transmitted infections. But it only does the job in a test tube. What we found in this study was that once you put N-9 in a woman's vagina, it will also cut through the fat of her cells, which makes it easier for HIV to get into those cells. Women who are highly exposed to N-9 actually show ulceration on the tissues of the vagina, and those ulcers can enhance the ability of HIV to get in. The same holds true for men. The rectum is even more vulnerable than the vagina to the effects of N-9.

Many experts still recommend N-9 as a contraceptive for women at low risk for contracting HIV. Do you agree with that?
I think if a woman is not using N-9 very often, there probably is a low risk of ulceration. It's not a perfect birth control method anyway, of course. But I really think that people should be using condoms all the time to make sure that they're safe.

There are a lot of condoms produced today that contain N-9. In light of recent findings, is this likely to change?
There has been a move to urge condom makers to take N-9 out of their condoms. Studies have shown that if you're using a condom correctly, the additional protection you get from N-9 in terms of preventing pregnancy is negligible, plus you're running the risk of increasing the transmission of HIV. We feel that adding N-9 isn't worth it, given the risks involved.

What is the state of HIV infection in the United States today?
We estimate that there are about a million people infected in the United States, of which only about two thirds know that they're infected. The number of new infections each year has remained quite stable for the last four or five years, at about 40,000 new infections each year. The thing is, the proportion of those who are women is rising precipitously. And the proportion of those who are African American is also rising, so a disproportionate share of the new infections are occurring in women, African Americans and Latinos.

Do we know why?
That's a really tricky question. Our prevention messages may not be working equally well in every community. Obviously, we need renewed efforts, new ways of tackling the problem, and new ways of communicating with diverse ethnic and age groups.

Do you think that the failure of N-9 to produce positive results will dampen hopes for a product that really works against HIV?
I hope not. After all, we had a promising product, we tested it, and we learned that nonoxynol-9 doesn't work. We also learned why, which means that we learned what we shouldn't be trying in the future. Now we have a better idea of what we should be looking at. Researchers are looking at different classes of chemicals that could disable HIV in completely different ways while leaving the vaginal and rectal lining intact.

Club Drugs and HIV: The Agony and the Ecstasy

Statistics show that people who take club drugs like methamphetamine, also known as crystal, may wake up with a big problem: HIV infection.
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Boosting HIV Awareness With New Test

Traditionally, getting tested for HIV has been a two-step process: arriving for the test, and returning a week or two later for the results. But the Food and Drug Administration (FDA) has approved a test that provides results in just 20 minutes, and the availability of this test could have a profound effect on HIV awareness and prevention efforts worldwide. Learn about this new HIV test and why everyone should get tested.
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Boosting HIV Detection With a Quick Test

By: Jeffrey Laurence, MD

Traditionally, getting tested for HIV has been a two-step process: arriving for the test, and returning a week or two later for the results. Approximately 8 to 10 thousand people tested in the United States each year do not make it to that second step. According to the Centers for Disease Control and Prevention (CDC), in the year 2000, those who did not return for results included 30 percent of the people who tested positive, and 39% who tested negative.

In November of 2003 the Food and Drug Administration (FDA) approved a test that provides results in just 20 minutes, and the availability of this test could have a profound effect on HIV awareness and prevention efforts worldwide.

Dr. Jeffrey Laurence is the Senior Scientific Consultant for Programs at the American Foundation for AIDS Research (amFAR), and Director of the Laboratory for AIDS Virus Research at Cornell University's Weill Medical College. In the following conversation, he describes how the test's quick results could boost awareness of HIV status, and, along with counseling, radically improve HIV prevention efforts.

First, what are the drawbacks of conventional testing?
The major problem is the time that it takes. It could take anywhere from one to two weeks to get the results. Also, you have a tube of blood drawn. Some people are upset about this if they haven't had it done before. It's also expensive. If you are tested in a hospital, versus a public clinic, the whole process could be anywhere from $50 to $100.

What is the rapid test and how effective has it proven to be?
It's called the OraQuick test. It only requires a few drops of blood (taken with a finger prick), and it takes about 20 minutes to get results. The rapid test is supposed to be virtually identical in sensitivity and specificity to the standard test that may take over a week to get the test results back. And I suspect that the rapid test will cost about $20, which is a lot more affordable.

What are the implications of this rapid test?
There are several. I think the biggest benefit to public health and to patients is the speed of results. People get nervous, come in, get their blood drawn for the regular test, and never come back for the test results. With this rapid test, we'll be able to capture those people, because they will certainly sit there for 20 minutes and wait for the results. If it's a positive test, they'll need to come back for a confirmatory test, but as this is a very accurate test, presumably there will be very few false positives.

And those individuals who test positive, presumably, will be given appropriate post-test counseling, will not spread the virus to other individuals, and will perhaps make a decision to see a physician about drug treatment. So in that sense I think it's a very important test.

Are there downsides to the test?
The test is relatively easy, and we obviously don't want it to be abused. We don't want people to just decide that because the test is so rapid, we're not going to offer any counseling. We don't want, for example, some employer to decide to start testing employees or, people to start testing their lovers or friends.

I can't think of any downside with normal use of this test, but abuse could come in if there is failure to provide counseling or if the test is used illegally. There must be safeguards.

Do you think this test will become the conventional test for HIV?
I think this test could supersede the conventional test, yes.

How can people find a site that offers this test?
At this moment there are 40,000 sites, predominantly located within existing laboratory clinics and hospital clinics. You would need to call your local public health agency, the Board of Health, or go to your doctor, and they should know which doctors are associated with a hospital would have access to this test.

Who should be tested for HIV?
I think everyone should be tested for HIV. I think people going into a new relationship could be tested. Anyone that's had any potential risk factors for this disease should be tested. Clearly, our biggest emphasis should be on high-risk populations -- men who have sex with men, injection drug users, sexual partners of men who have sex with men, or sexual partners of injection drug users, people who have had multiple blood transfusions. People who have had other sexually transmitted diseases are at risk for getting HIV.

I would like to see this HIV test used routinely, and made part of a normal medical history. If there are any risk factors for HIV disease, the test can be offered, and because it's so quick, it could be offered right there and then.

There are lots of reasons why people don't want to be tested. But now we have effective treatments for the HIV virus. Many people are living long lives with HIV, and people should know that we have treatment options available if we tell them they're HIV positive.

Introduction to HIV

This article offers a broad overview of the human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS). It describes how the virus is contracted, how it behaves in the body, and what is involved in HIV testing.
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Introduction to HIV

By: Brian A. Boyle, MD

What are HIV and AIDS?

The Human Immunodeficiency Virus, which is commonly called HIV, is a virus that directly attacks certain human organs, such as the brain, heart, and kidneys, as well as the human immune system. The immune system is made up of special cells, which are involved in protecting the body from infections and some cancers. The primary cells attacked by HIV are the CD4+ lymphocytes, which help direct immune function in the body. Since CD4+ cells are required for proper immune system function, when enough CD4+ lymphocytes have been destroyed by HIV, the immune system barely works. Many of the problems experienced by people infected with HIV result from a failure of the immune system to protect them from certain opportunistic infections (OIs) and cancers.

Defining the terms
People infected with HIV are broadly classified into those with HIV disease and those with Acquired Immunodeficiency Syndrome, or AIDS. A person with HIV disease has HIV but does not yet have any symptoms or related problems, and still has a relatively intact immune system (that is, a CD4+ lymphocyte count greater than 200 cells/mm³). A person with AIDS, on the other hand, has very advanced HIV disease and his or her immune system has incurred significant damage. As a result, people with AIDS are at very high risk for a number of OIs, cancers, and other AIDS-related complications. The Centers for Disease Control have defined the conditions that mark a progression from HIV disease to AIDS. They are:

certain infections, such as repetitive pneumonias, Pneumocystis carinii pneumonia (PCP), and cryptococcal meningitis
certain cancers, such as cervical cancer, Kaposi’s sarcoma, and central nervous system lymphoma
CD4+ count less than 200 cells/mm³ or 14 percent of lymphocytes

How AIDS Works in the Body

Before highly active antiretroviral therapy (HAART) became available, most people who contracted HIV eventually progressed to AIDS and had some AIDS-related complication, such as:

a deterioration of immune system function and an increased risk of infections and cancers
brain damage that may cause dementia or memory loss
heart problems that can cause heart failure and symptoms such as shortness of breath, fatigue, and swelling of the abdomen and legs
severe kidney damage requiring dialysis
an inability to perform activities of daily living such as balancing a checkbook or driving a car
metabolic changes that may cause significant weight loss or diarrhea

Due to these potential problems, a person with AIDS is at very high risk of becoming very ill, and, if some action is not taken to protect the person from these infections or reverse the damage done by HIV, he or she is at risk of dying.

The speed of progression to AIDS
The damage caused by HIV occurs more quickly in some people than in others, but generally an untreated HIV-infected person can expect that they will progress to AIDS within 10 years of their infection. During the time the person is infected with HIV, a war rages between the person’s immune system and HIV, with HIV slowly wearing the immune system out.

A slow progress: A number of factors can affect how rapidly HIV progresses, some that can be controlled, and some that can’t. Some people have certain genes that slow HIV progression, or they are infected with a weak strain of HIV that their immune system is more able to control. In general, taking better care of yourself and following your doctor’s advice also slows the progression of HIV disease to AIDS.

A more rapid progress: Factors that may cause a more rapid progression to AIDS are: infection by a virulent strain of HIV, having a high viral load setpoint (a certain level of HIV replication that varies from person to person), older age, and the abuse of drugs or alcohol.

HIV Treatment

In the time between initial infection and AIDS, the infected person may feel relatively normal, despite the constant attack by HIV. People living with HIV have to understand, however, that despite feeling well on the outside, significant damage can be occurring on the inside. Fortunately, over the past five years, significant progress has been made regarding the treatment of HIV and prevention of some of the infections and cancers that may be caused by it. Antiretroviral medications can directly attack HIV and stop it from reproducing and causing further damage. For most people, the biggest factor in preventing progression to AIDS is adherence to HAART, which can suppress HIV replication to very low levels and not allow it to continue to attack the body.

Prophylactic medications
In addition to HAART, other steps can be taken to prevent illness in people living with HIV and AIDS. Certain antibiotics, called prophylactic medications, can effectively prevent opportunistic infections. A physician can help to assess the appropriateness of these medications in a particular treatment program, and which ones to use, but it is important that they be taken as prescribed so that infections can be prevented. With careful monitoring, OIs and certain cancers can be detected in their early stages before they have spread, and the antibiotics can work more effectively to ward off further serious complications. I recommend that every person living with HIV or AIDS see a physician for appropriate monitoring and treatment.

Who Should be Tested for HIV?

In the early 1980s, when HIV infections were first starting to appear, HIV was associated primarily with gay men. Then it became associated with intravenous drug users and hemophiliacs. During the past 20 years, however, HIV has become a disease that can affect almost anyone who is not monogamous with an uninfected person.

HIV contraction
HIV is contracted through an exchange of bodily fluids, such as blood, semen, or vaginal secretions. As a result, the most common ways of acquiring HIV are sharing needles while doing intravenous drugs, and sex, especially anal intercourse. While the highest risk of HIV transmission is associated with anal intercourse, vaginal intercourse is becoming a common means of spreading HIV. Vaginal intercourse is the most rapidly growing risk factor for acquiring HIV infection in the United States and in the developing world it is the most common method of HIV transmission. Everyone must take appropriate steps to prevent the spread of HIV: Safer sex with condoms and dental dams and not sharing needles can help prevent the spread of HIV.

Common misconceptions about contraction
People are often concerned that HIV can be contracted through common contacts with an HIV-infected person, such as shaking hands or sharing glasses or eating utensils. These are not risk factors for contracting HIV. There is no evidence that HIV can be spread through these means, and people should not be afraid to be around people who have HIV or to use a glass, eating utensils, or plate that an HIV-infected person has used, or to have other common contacts.

Those who should consider being tested for HIV include:

people who received a blood transfusion or blood product at any time, but especially in the late 1970s or 1980s
homosexuals and heterosexuals who have a history of unprotected sex with potentially infected persons
people who have had multiple sex partners
people who have had a sexually transmitted disease such as syphilis or gonorrhea
people who are intravenous drug users
pregnant women

The importance of testing and diagnosis
The importance of testing and diagnosis has increased over the past five years. Before the improvements in antiretroviral therapies, many people believed that there was little that could be done to prevent the progression of HIV and so they did not get tested. While these people were right about the ineffectiveness of the antiretroviral therapy available at that time, they failed to recognize that medicines had been discovered that could prevent many of the common infections that afflict AIDS patients. Thus, many people were diagnosed with HIV only after they were admitted to the hospital with severe infections, especially PCP. Some died needlessly because they had not sought appropriate medical care and did not receive one of the medications that could have prevented PCP from occurring.

Now, there are even more reasons to seek HIV testing and medical care. Within the past five years, the medicines to prevent infections have been significantly improved and effective antiretroviral therapies have been developed that can not only halt the progression of HIV, but can also reverse much of the damage that has already been done. Therefore, it is important that HIV is diagnosed while the person is relatively healthy and before a major, potentially life-threatening OI occurs, such as PCP or cerebral toxoplasmosis. With HIV, what you don’t know can hurt you.

If you think you are at even slight risk of having HIV—if you have had numerous sex partners or if you have had sex with someone who might have been bisexual or had a history of intravenous drug use—you should be tested. If you test positive, you can then receive medical care necessary to keep you healthy and prevent the diseases that occur in untreated AIDS patients. If, on the other hand, you wait until you feel sick before you are tested, you may already have progressed to AIDS and your immune system may already have incurred significant damage that may not be reversible.

Pregnant women
Recent advances in therapy have also led to effective methods of preventing mother-to-child transmission of HIV. Virtually every pregnant woman, especially those who have a history of intravenous drug use, have had sex with someone in a high-risk group, or who have had numerous sexual partners, should be tested for HIV. HIV-infected mothers should consider taking antiretrovirals, which can effectively prevent transmission to the infant. Since breast-feeding can also cause transmission of HIV to the infant, HIV-infected mothers should not breast-feed their infants if there is an available alternative. Many states also require testing of the infant at birth, so that appropriate treatment can be provided.

Testing is voluntary and confidential
Under most circumstances, HIV testing is voluntary. Unless there are special circumstances, most states require a person to give specific permission, called informed consent, before he or she can be tested for HIV. Privacy and confidentiality are legitimate concerns for people who are being tested for HIV. Most people do not want other people or organizations, such as their employer, to know they are HIV-infected and most don’t even want them to know that they are being tested. Most states have laws that protect the confidentiality of HIV testing and the diagnosis of infection. While accidental disclosure of a person being HIV positive can occur, in my experience it is extremely rare. It’s a mistake to avoid testing because of fear of accidental disclosure.

Also, there are other options including anonymous testing in a clinic or at home (for example, Home AccessR), where you are identified by a number, not by name, and no one but you knows your number. The cost of testing is generally between $30 and $100, and some groups, including many health departments, provide testing free of charge.

How Does HIV Testing Work?

HIV is usually diagnosed by a blood test, but newer tests can be done on saliva or urine. If you’re squeamish about getting blood drawn, there are alternatives you can discuss with your doctor. Generally, the purpose of the test is to search for antibodies to the virus. The initial test is an enzyme-linked immunoabsorbent assay (ELISA) and is confirmed using a test called the Western Blot. The antibody tests are very reliable, but may not be able to detect an infection during the first six months after an exposure. There is also a test that can test for the presence of the virus itself, and this test is called an HIV PCR. HIV PCR is used to test for HIV after a potential HIV exposure, but before antibodies have developed. Because infants may have their mother’s antibodies in their blood confounding the HIV antibody test, HIV PCR is also useful for them. However, HIV PCR may not be reliable in detecting HIV in all infected patients, especially those with a low viral load.

How long do the results take?
It used to take several days to a week to get test results back. Now there are rapid detection methods that allow reliable results in less than an hour. As a result, HIV testing can be completed while you are still in your doctor’s office.

Test counseling
Pre-test and post-test counseling and education are important parts of HIV testing. Counseling gives people who test negative for HIV an opportunity to learn more about HIV and how to avoid becoming infected. For those who test positive, counseling gives them a chance to learn about the importance of being medically evaluated and, if appropriate, treated so as to prevent disease progression or OIs. These counseling sessions take about 15 minutes, including time for questions. They are a very valuable part of the testing process, regardless of the test results.

Conclusion

HIV disease is a chronic disease that used to be fatal for virtually everyone who got it. Now, things have changed and effective treatments are available to treat HIV and, in most cases, these treatments can prevent HIV from doing further damage and can keep the person healthy. In order to take advantage of these treatments, you must be tested and diagnosed with HIV. All persons who may have been infected with HIV and virtually all pregnant women should be tested as soon as possible.

Advice to Patients Recently Diagnosed With HIV

HIV treatment has come a long way since the first reported case of AIDS in 1981, and today there are a number of effective therapies available to people living with HIV. This article explores how people who are newly diagnosed with HIV can take an active role in their own treatment, and the maintenance of their own health.
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Advice to Patients Recently Diagnosed With HIV

By: Bruce Olmscheid, MD

Introduction

Being infected with HIV is no longer a death sentence. HIV is now looked on as a chronic manageable condition. However, having HIV is no picnic, either. Like diabetes, it can cause complications if not treated appropriately. The more you learn about HIV and how you can take an active role in treating it, the more likely it is that you will remain healthy and free of complications. To remain healthy will require your active participation.

Based on our knowledge of HIV and the treatments currently available, having HIV means being infected for the rest of your life. We are hopeful that research will lead to a cure for HIV, but that cure does not exist yet. There have been dramatic advances in the treatment of HIV during the past five years. These advances will, without a doubt, continue to develop at a very rapid pace. Although you may need to be on some type of treatment for a long time (perhaps for the rest of your life), the specific treatment you and your healthcare provider choose now will most likely change as we learn more about HIV, HIV treatments, new drugs, and new drug combinations.

Effective Management of HIV

After learning that you are HIV-positive, it is important to see you doctor regularly. This usually means every two to three months, though your initial visits may be more frequent than that. During this time you will learn a lot about HIV and treatment options that are appropriate for you. Also, during these initial visits you will learn about T cells, the immune system and your viral load. You will learn how these numbers are used to determine whether you should start treatment early or defer to a later date. Regardless of what choice you and your doctor make, it is important that you see your doctor regularly to monitor the state of your immune system. These visits to your doctor will also allow you to learn about new developments in the treatment of HIV.

When to Start Treatment

Before you decide which treatment is appropriate for you, you will have blood tests done to determine whether it is recommended that you begin treatment now, or if you may safely defer treatment to a later date. The treatment guidelines have evolved and changed as we have learned more about HIV and response to treatment. For example, three years ago most experts agreed that anyone with HIV should be treated aggressively as soon as the diagnosis was made. This has been referred to as "Hit Hard, Hit Early." This one-size-fits-all approach is no longer applicable.

Blood tests will determine the number of T cells (the CD4 count) and the amount of virus (the viral load or HIV PCR RNA or HIV bDNA) in your blood. These numbers will help to determine whether it is safe for you to continue to be monitored without medication (antivirals or antiretrovirals) or whether you are at high risk of becoming sick from HIV and would benefit from starting these medications now.

Choosing an Initial Antiviral Regimen

If you and your doctor agree that it is safe to monitor your blood tests without treatment, it is important that you have these blood tests done regularly. This means usually every three months.

If your numbers suggest that you should begin treatment, you and your doctor will discuss options that are available to you. There are many approved medications available and many others in advanced stages of research and development. These medications are used together in groups of three or four medications often referred to as a cocktail. It is important that your doctor be an expert in the use of these medications. You do not need to become an expert, but the more you learn about HIV and how these medications work to suppress HIV, the better you will do with treatment.

Adherence to treatment regimen is key to success
The most important thing you should understand at this point is that you must be ready to commit to treatment exactly as prescribed by your doctor. If you start a treatment regimen but do not adhere to your prescribed medication schedule, the virus will have an opportunity to develop resistance to the drugs, and will not be completely suppressed in your body. It is extremely important that you understand this concept. If you do not understand what this means, or feel that you are not ready, you must discuss this with your doctor. You can easily do more harm than good if you do not take the medications as prescribed.

Learn About Side Effects

Each drug and each drug class has side effects that may occur shortly after starting the regimen. Many of these short-term side effects diminish within a few days or weeks of starting the regimen. Your doctor can give you important advice on how to manage these side effects. Some drugs have the potential to cause some serious side effects that can be life threatening. It is important that you be aware of the signs and symptoms that you must look for and report immediately to your doctor. These serious side effects are rare, and hopefully fear of them will not prevent you from starting therapy.

We are learning more about the long-term side effects of therapy as well. It is not clear whether some of these effects are due to HIV itself, one or more of the drugs, or a combination of both. Many people worry about these long-term effects. It is important that you discuss this with your doctor also. Clearly, allowing HIV to progress to AIDS is much more serious and life-threatening than any of these other side effects that may occur.

Get Vaccinated for Preventable Infections

Whether you start therapy or determine that it is okay for you to defer therapy, your doctor will recommend a series of vaccinations or immunizations. These are just like the shots you received as a child to prevent you from acquiring measles, mumps, tetanus, or other common viral infections. It is important that you receive these shots, as they help to prevent infections that could later tax your immune system or cause serious and life-threatening illnesses. This series of shots can take up to six months to complete. It is important to keep your appointments to receive these shots on time.

Take Precautions to Prevent Spreading HIV to Others

Once you know you have HIV, you will probably have questions about steps you can take to reduce the risk of spreading the virus to other people. Your family, sexual partners, and roommates may have significant concerns about this also. You and your doctor will review safer sex guidelines. Sex can be difficult to talk about, but it is important that you understand safer sex guidelines, and ask any questions you may have. Sexual activities that result in the exchange of body fluids lead to a higher risk of transmitting HIV. Other sexual activities are less likely to transmit HIV. Your doctor should discuss safer sex practices with you in detail.

In addition to having safer sex, you must not share needles. Although controversial, needle exchange programs have gone a long way to reduce the spread of HIV in people who use IV drugs.

Since HIV is spread very easily through blood and blood products, anyone with HIV infection will not be able to donate blood.

There are many fallacies about how HIV is spread. For example, some people still believe that you can get HIV from someone by eating off of the same plate, using the same glass, or sitting on the same toilet seat. These are not ways that HIV is spread.

Keep Your Immune System Strong

A number of common-sense issues are important. Get plenty of rest, eat a well-balanced diet, and exercise regularly. Avoid excess amounts of alcohol, and if you smoke, you will do yourself a favor by stopping. There are medications that help increase your chances of stopping and "staying stopped." Ask your doctor if those medications are appropriate for you. Avoid the use of recreational drugs.

Take an Active Role in Treating HIV

Find a doctor or healthcare provider who you feel comfortable with. Realize that you will be living with HIV for the rest of your life. Prepare yourself to learn about HIV and HIV treatments. You do not need to devote your life to HIV unless you choose to. You cannot learn everything overnight. There are many sources of information about HIV. Find the ones that work best for you.

Find someone to talk to
Many people feel that they do not want anyone else to know that they have HIV. As time goes on however, most people do find at least one or two people that they feel they can trust. It is important to find support from someone. If not someone close to you, consider a support group or online group. Your doctor or social worker can often help you with finding support. These sources of support can help you feel less alone. It can be very reassuring to know that others have gone here before you.

Conclusion

HIV infection is now a manageable, chronic infection in many cases. The more you learn about HIV and the steps you can take to control it in your body, the more likely you will live a normal, healthy life.

Changes In The HIV Epidemic: What Do They Mean For You?

Changes in the HIV epidemic receive widespread reporting in the media. For people living with HIV, following the news about new research and treatment can be enormously confusing. Reports of new treatments may stir doubt in individuals about the efficacy of their current treatment. This article outlines how advances in HIV research have affected individual HIV cases, and how people living with HIV can make sense of new information about the virus.
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Changes in the HIV Epidemic: What Do They Mean for You?

By: Simon Paul, MD

Introduction

Changes in the HIV epidemic receive widespread reporting in the media. Everyone wants to know if people are still catching HIV, if people are still getting sick from HIV, if antiretroviral medications are still working, and so on. All of these questions are vitally important, and data about the whole population help give us the answers. In addition, the guidelines for antiretroviral treatment are based in part on such data, as are decisions about how to use resources to fight HIV. However, what is happening to the average patient, or the epidemic as a whole, may or may not be what is happening to you. You can learn from another patient's stories of successes or problems with HIV, but still have to remember that your own experience will be unique. Here, we will look at what changes have been reported for people with HIV both before and after effective antiretroviral therapy, and what these changes mean to individuals with HIV.

Prophylaxis for Opportunistic Infections

Even prior to the introduction of highly active antiretroviral therapy (HAART), there were improvements occurring in the health of patients with HIV. The decreases in death rates from AIDS that were widely reported after the introduction of HAART actually began prior to HAART. All of the reasons for this pre-HAART improvement may not be known, but a number of factors were probably important. Improved ability to prevent, to recognize, and to treat opportunistic infections (infections that flourish because of the impaired immune system in patients with HIV) played an important role. The increasing use of Pneumocystis carinii pneumonia (PCP) prophylaxis prevented a large number of hospitalizations and deaths. As large studies testing medications for Mycobacterium avium complex (MAC) were completed, the infection changed from being untreatable, to treatable, to preventable. What did these changes mean to a patient with HIV? If your T cells were low, leaving you more susceptible to infection, these changes were very important—the methods to prevent opportunistic infections were becoming increasingly clear. On the other hand, if your T cells were high and your immune system was normal, or close to normal, these changes did not benefit you, though they might in the future when your T cells dropped.

Two-Drug Regimens

Other changes prior to the widespread use of HAART also may have led to the initial declines in AIDS death rates. While not highly active like the three-drug regimens we use currently, two-drug therapy, for example with didanosine (ddI) and zidovudine (AZT), was demonstrated to be active in several studies. These two-drug regimens, while less durable than the current regimens, were effective in preventing both illness and lowered T-cell counts. Clearly, it was encouraging news that something was effective at treating HIV and not just preventing infections. Many of my patients were able to survive and avoid illness by using these regimens.

Prior to HAART, and even now, the most important question is whether to start therapy or to wait for something better to come along. Thinking back to the time when two-drug regimen clinical trial results became available can help put this question in perspective. We now know that two-drug regimens are not durable and can lead to drug-resistant HIV. But when the initial good results of two-drug therapy became clear, patients and their doctors had to decide whether to begin two-drug therapy or to wait. The logical answer seemed to be that if patients in the clinical trial improved and were healthier on two-drug therapy, then one should start the therapy.

When it comes to making important treatment decisions based on clinical trial results, there are several questions you have to ask yourself before leaping to the conclusion that successful results in clinical trials mean successful results for you.

Are you in the same situation as the people in the trial? For example, say the trial showed that T-cell counts improved or stopped declining. Well, how stable are your T cells? If yours are not declining, perhaps your health situation is different than those in the trial. Say the trial demonstrated fewer opportunistic infections and deaths. That is extremely important, but if you are not at risk for opportunistic infections or death at the moment, perhaps you will not have the same benefits as the people in the trial.

How long did the trial last, and can you predict how the people in the trial will do further along?

Is this all the information you will have to make your decision, or will there be more information soon that will make the decision easier?

What about the duration of the trial? If it lasts for three or four years and that sounds like a long time in your current state of health, then your long-term questions are largely answered.

Can you predict the long-term outcomes for these trial patients? Predicting long-term outcomes for trial patients is perhaps the most uncertain issue to consider. If you have questions about the long-term effectiveness of a treatment, how important are these questions compared with your current need for treatment?

It is important to keep these questions in mind. Obviously, long-term results of clinical trials are not known for certain for quite some time. However, you can ask how well patients are doing on a proposed therapy, why they stop, what side effects occur, and if there are any clues as to how they will do in the future. These answers may help you make decisions for your own treatment.

Keep abreast of HIV treatment information
The possibility of having new information in the future that will help you make decisions is very important, and I am surprised by how frequently this possibility is ignored. The medications for HIV have improved immensely and continue to improve. Our knowledge of how to use antiretroviral medications effectively is also improving, as data from clinical trials continue to be reported. So you should keep in mind that delaying therapy could mean better or easier therapy in the future.

Delaying therapy
How does delaying therapy versus immediately starting therapy play out for an individual patient? That can be a complicated question. For example, it is likely that starting therapy when your T cells are high leads to a better response. However, if you wait for a year during which time a simple once-a-day regimen is developed that greatly improves your chance for adherence (your ability to take every dose of medicine without missing doses), it's quite likely that the disadvantages of starting therapy at a slightly lower T-cell count would be outweighed by the improved adherence. While your doctor can discuss the risks and benefits of this hypothetical situation, it is ultimately up to you to decide if this easier adherence would be important to you and worth the risks of delaying therapy.

The Beginning of HAART

With the introduction of HAART, there were reports that people were feeling better and returning to work. This led to natural hopes that a cure was in sight. There was enormous publicity regarding dramatic decreases in deaths, opportunistic infections, and increases in T-cell levels. During the course of a year or two, about 70 percent of patients in many large HIV centers had begun HAART. While there have always been people who had serious problems with side effects or drug resistance, most people got off to a good start. They did feel better than they had, or, if they were asymptomatic, their T-cell levels increased and it was an enormous boost to see things improving. For most patients, the good news in the media matched their own sense of well-being.

Today the reports are starting to change. This can lead to a lot of confusion for patients-"If others are having problems does that mean I will have those same problems?" A natural question, but once again, you have to assess your own situation, which may not be similar to another patient's.

Recent Trends in Treatment

What are the most recent trends for HIV patients? They seem to be heading in two directions. Medications are becoming easier to take and yielding better results. On the other hand, the problem of adherence is starting to demonstrate its importance, as some people who benefited initially from HAART develop an HIV virus that is resistant to one or more medications. In one "real-world" study (as opposed to a clinical trial) using largely protease inhibitor-based therapy, only 40 to 50 percent of patients managed to maintain the goal of an undetectable viral load—which demonstrates the difficulties in maintaining adherence outside of the motivation of a clinical trial.

Not all health problems are caused by HIV
The problems of cross-resistance between HIV antiretroviral medications are also becoming clearer as salvage therapy trials show only 20 to 40 percent response rates. The effects of antiretroviral therapy failure may be part of the reason for recent reports of a stop in the decline of HIV-related deaths and hospitalizations. The combination of these findings has made many patients pessimistic about starting or continuing their therapy. However, deaths and hospitalizations amongst HIV-infected patients are not only due to HIV. Reports indicate that other problems such as hepatitis C and liver disease are increasing causes of illness. There are also increases in HIV-related cancers such as central nervous system (CNS) lymphoma. The risk for lymphoma goes up as T-cell levels go down, therefore most people with CNS lymphoma have less than 50 T cells. In the past, a lot of people with low T-cell levels died from opportunistic infections before they had time to develop lymphoma. Now, they live longer on HAART, and perhaps with more time alive, have more of a chance of developing lymphoma. These days, patients usually start HAART before their T cells get that low. It's possible that if your T cells never drop below 50 you're not at risk for CNS lymphoma and you will not be likely to develop it while on HAART.

Each patient is different. Trying to compare yourself to this nonexistent average patient can be increasingly misleading. Clearly today, average patients include patients for whom HAART has not continued to be as successful as hoped. These patients have high viral load values and often declining T-cell counts. The average also includes patients doing fairly well on HAART, who are now having problems related to liver disease, heart disease, or other conditions. The average also includes patients who have started HAART, who have had no problems with the medications, have good adherence (perhaps to a newer, easier-to-take regimen), and who continue to improve clinically.

What Patients Can Do to Help Themselves

With such a mixture of problems, what can you learn that will be helpful to your own health? First, think through why some people are having problems and what you can do to prevent having the same trouble. Are they having problems from hepatitis C? Well, find out your own hepatitis-C status and if treatment would benefit you. Are patients developing HIV that is resistant to medications? Try and find out why and what you can do to improve your own medication adherence (non-adherence can create drug-resistance in some cases). Are people getting sick from side effects? Find out what side effects, and from which medications. Investigate what you can do to keep from developing these problems. For example, if a patient in the waiting room tells you stories of neuropathy or nausea, or of lipodystrophy/fat redistribution syndrome, do not assume that you will have the same problems. You may not even be at risk on your current medication regimen for some of the side effects that you fear. But do find out what you can do to avoid them, or to detect them early if you are at risk. If you hear in the news that antiretroviral medications are failing in 50 percent of patients, does that mean the other 50 percent are about to fail? Not necessarily. You need to know what to do to increase your chances of being in the 50 percent who are succeeding. Or possibly, given your current situation, studies of patients beginning treatment are not so relevant to you. If you have low T cells and a high viral load, despite being on HAART, and are without any great options, perhaps, in clinical terms, you are still doing better than before. You need to be learning about future treatments that may benefit you and not worrying about the success rates of people who are just beginning medications.

Conclusion

HIV and AIDS receive a lot of attention in the media. Frequently the data are made excessively dramatic for the news. The results may be presented in the most negative or most positive manner possible. For patients, this skewed reporting may lead to a lack of interest in treatments that could be beneficial, or sometimes, an interest in treatments that should be avoided. Whether the information is positive or negative, there is often much that you can learn from it to improve your own health. Do not shy away from finding out more about "bad" news, and do not jump too readily to accept "good" news. Bad news could become good news if you can use it to prevent a problem, avoid a side effect, or change your treatment plan to keep your own health on the course you choose. Use both good and bad news as a means to increase your understanding about HIV, HIV treatment, and about your own unique health situation.

HIV Prevention

Recent statistics report that there are over 5 million new cases of HIV reported annually. This article stresses the importance of prevention, and outlines prevention techniques. For those who are HIV positive, the article describes ways to prevent spreading the disease to others.
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Choosing a Healthcare Provider for HIV Treatment

Receiving an HIV diagnosis can be devastating. But if you have just been diagnosed, it is important to begin working with a healthcare provider on a treatment plan soon after diagnosis. This article outlines some useful considerations as you choose a new healthcare provider, and details what you should expect from your doctor as you work together on a treatment plan.
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Choosing a Healthcare Provider for HIV Treatment

By: Brian A. Boyle, MD

Introduction

If you are newly diagnosed with HIV infection, this may be a very difficult time for you. Many newly diagnosed patients have severe bouts of depression and anxiety. They simply don’t know where to turn or what they should do. This may lead to denial, procrastination, and avoidance. If you feel like this and have not taken steps to seek treatment, this understandable, but unfortunate behavior may be not only detrimental to your health and well being, but also may deny others the opportunity to be tested and treated or may lead to further spread of HIV through continuation of unsafe sex practices or needle sharing.

The Decisions

There are several decisions you have to make in order to be sure that you are doing what you can to:

prevent the spread of HIV
prevent the progression of your HIV disease to AIDS
avoid getting sick or perhaps even dying

If you are engaging in high-risk behaviors, the first decision you need to make is to stop engaging in these behaviors, as they may endanger others and cause them to become infected. This means that you must not have unprotected sex (a condom or dental dam are required at all times to prevent direct contact) and, if you use intravenous drugs, you must not share needles with other people. The people with whom you have had sex or shared needles in the past may or may not already be infected. You should consider informing them yourself of their exposure to HIV, but if you are unable to do so, you should contact your doctor or the health department so that the people with whom you have had sex or shared needles can be informed anonymously and then get tested. If you have children, they may also need to be tested, but you can discuss this with your doctor as well.

Choosing a Healthcare Provider

This decision involves first assessing your healthcare options, gathering some information about providers, making a choice, and scheduling an appointment. Keep in mind that your contact with the healthcare provider you choose will be confidential and that your provider will not release information about you unless you tell him or her that it is all right. Remember, just because you visit one healthcare provider doesn’t mean you have to stay with him or her. If you don’t feel comfortable with that provider or you don’t like him or her, then you should continue your search and go see another provider. If you are a part of an HMO, you may need to pick a doctor from the list of providers in your HMO or you may be referred to an HIV specialist by a primary-care doctor. Someone at your health plan should be able to provide you with information about how to find an HIV specialist so that you are able to have several choices.

The medical qualifications
Healthcare providers include physicians, physician’s assistants, and nurse practitioners. Physicians have been to medical school, followed by a residency in internal medicine or family medicine, and in some cases, a fellowship in a subspecialty such as infectious disease. Nurse practitioners and physician’s assistants have not been to medical school nor have they done a residency or fellowship, but they have received a substantial amount of education and training and in some states, they are allowed to treat patients without physician supervision.

Some people feel more comfortable with a doctor, while others feel more comfortable with a nurse practitioner or physician’s assistant. You can receive excellent care from any of these healthcare providers so long as he or she is well versed in treating HIV disease and has adequate experience. This is an important attribute to remember, as several studies have shown that physician experience plays a major role in how well a person with HIV disease does, including whether they get sick and how well they take their medications.

Support staff
Also, it is important to keep in mind that when you choose a healthcare provider you are also choosing that person’s support staff and system. Since there are a number of social issues and questions associated with HIV disease, you want to make sure that the doctor has someone on staff or someone to whom he or she can easily refer you who can help you take care of insurance and billing issues, drug or alcohol problems, disclosure issues, and other concerns that patients with HIV disease frequently must confront. These issues are complex and frequently require expert assistance from a very knowledgeable person. You are going to have enough to deal with. You should not have to be constantly struggling to get the benefits and help that you need.

Getting the provider you want
Since you are unlikely to know many healthcare providers, one of the biggest questions you might have is, "How do I find the healthcare provider that I want?" You can start by asking relatives and friends, especially those who are HIV-infected. If your family and friends do not yet know about your HIV infection, before approaching them, you should consider whether or not you want them to know. If you don’t, there are other ways to find a doctor. You can call a local medical society or a local patient advocacy/support group. For example, you could call a Gay Men’s Health Crisis center in your area or a methadone maintenance clinic. You could also call a local hospital. They may be able to provide you with a list of the experienced healthcare providers in your area. Additionally, you could ask your current healthcare provider to refer you to an HIV specialist (i.e., someone who treats a significant number of HIV-infected patients).

If you cannot find a provider with adequate experience in your city, consider contacting services in larger cities that may be nearby. Some of my patients travel quite a distance to see me because they could not find anyone locally with whom they were happy and our center provides not only excellent healthcare, but also provides them with access to new treatment studies and the support services HIV patients need.

Doing research
Once you have identified a potential healthcare provider, consider calling their office and getting information about:

the number of patients they treat
the number of years they’ve been involved with HIV
their educational and training background
any support staff they can provide for you (e.g., social worker, psychiatrist, nutritionist)

Scheduling an appointment
If you are satisfied with the preliminary information, then schedule an appointment for an initial visit. If not, keep looking. I can assure you that with a little effort you will be able to find an excellent provider who will be able to meet your needs.

The Initial Visit

The initial visit can be frightening and intimidating, but you should keep in mind that the entire purpose of the visit is to provide you with the medical and other help you need to control HIV infection. You may not feel very comfortable during this visit and a lot of things will be happening, but you should try to assess whether you will eventually be comfortable in this setting, receive the support and services you need, and have confidence and trust in your healthcare provider.

The paperwork
Your healthcare provider and his or her staff will guide you through the steps involved in the initial visit. This generally starts with a lot of paperwork, with which the staff can help you. This process will be smoother if you bring any insurance information or past healthcare records you might have with you. It will also help if you are on time or even a little early so that you have plenty of time and do not feel pressured or rushed.

Meeting with the healthcare provider
Usually, after the initial paperwork is completed you will meet your healthcare provider. He or she will often begin the meeting by obtaining a thorough medical history and doing a physical examination. This might include having blood drawn and sent to a laboratory for testing. He or she will provide you with a basic education and information regarding HIV disease, including the basic disease process and treatment options that are available. It is important that you tell your provider about any medical problems you have had in the past and if you are allergic to any medications.

Making a custom-fit treatment plan
You should use this time to discuss your treatment objectives with the provider. Every patient has different goals and ideas about their treatment. You should talk about these with your doctor and make sure that he or she feels comfortable with them and is not using a "cookie-cutter" approach, where every patient must do the same thing (for example, take antiretrovirals). Your doctor should show flexibility and adjust to your needs, while at the same time providing you with the education you need to make informed and knowledgeable decisions.

If you have not previously had a CD4+ lymphocyte and HIV viral load performed, the provider may not be able to provide any specific treatment details at this point, as he or she does not know how the virus has affected your body. Still, the provider should lay out the general approach that will be taken to control your HIV disease and to prevent opportunistic infections. You should feel free to ask questions and, if possible, to get written materials you can take home to read. If you already have strong feeling or beliefs about certain treatment options, you should specifically discuss these with your provider.

During this visit you should feel free to ask the provider any questions you may have about his or her medical background, and if these questions are met with hostility, you should be wary of this doctor. Your relationship with your healthcare provider must be based on trust. You will need to develop a rapport with your provider that allows you to feel confident about his or her medical advice, and feel confident making the important decisions about your own care.

Discussing disclosure
The provider may also take this opportunity to discuss disclosure issues (e.g., telling family members, telling others who might be at risk) and the need for you to seek additional help regarding depression, substance abuse, or other issues which may affect your health and healthcare. Again, this is a chance for you to share, with complete confidentiality, the concerns you have and problems you are experiencing. To have a trusting and supportive relationship with your provider is essential to maintaining your good health and you should take advantage of this rare opportunity to get things off your chest and get the help you need.

Conclusion

Choosing a healthcare provider to help you treat your HIV disease can be an overwhelming decision. However, it is also a very important one. Take the time to research and find the right provider and support staff for you. It will help you as you learn to manage your HIV disease and keep you healthy.

Transcript of the press conference with the Special Representative of the Secretary-General for Timor-Leste, Atul Khare for the visit of Dr Nafis Sadi

2008-02-18T20:54:00.000-08:00

http://www.reliefweb.int/rw/RWB.NSF/db900SID/EGUA-7BMMN3?OpenDocument

Good morning, before I depart for New York this afternoon to address the Security Council on the progress made and future challenges for UNMIT, I am particularly happy and delighted to be able to introduce Dr Nafis Sadik.

Dr Sadik is visiting Timor-Leste from 6-7 February to discuss the importance of, and raise awareness about HIV/AIDS issues.

Particularly, Dr Sadik is is here to raise awareness on the importance of focusing efforts on HIV/AIDS education and prevention campaigns before HIV/AIDS becomes a significant issue in Timor-Leste.

She has been involved with the UN for many years and in 1987 became the first woman in the history of the United Nations to be made head of one the UN agencies.

Dr Sadik is currently the UN Secretary-General Special Envoy for HIV/AIDS in Asia and the Pacific

She has worked and campaigned in the areas of reproductive health, population issues and family planning and has won numerous international awards and honours for her contribution to these fields.

I will now hand over to Dr Sadik for an opening statement and then we will accept your questions

Dr Sadik: Thank you very much. I have been here for just 24 hours, I am here as the Special Envoy of the Secretary-General for HIV-AIDS in Asia and the Pacific.

Asia and the Pacific is still considered generally as a 'low prevalence' area with a generalised epidemic in only a few countries. Within Asia, Timor-Leste is considered a low-prevalence country. And this is where in fact my role is very important as I have been tasked by the Secretary-General to convince leaders in low-prevalence countries that the time for action is now.

This means giving priority to HIV/AIDS and the way in which that this should be addressed. The leadership needs to speak out all levels about HIV-AIDS as a priority in all sectors of the society.

Secondly we need to have programmes for those most at risk, including men who have sex with men, commercial sex workers and their clients, and of course as a group, young people.

There have been many surveys and studies that show there is a lot of misconception and misinformation about how HIV may be transmitted. People believe it may be spread by mosquitoes, or sharing food with people and don't always know that it is a sexually transmitted disease or spread through the exchange of bodily fluids.

Condom use is very low by those in high risk groups and access to condoms for males and females is not high. I've had very interesting and positive discussions with the Government. For example, the Prime Minister agreed that he would be willing to speak out more and he wanted to understand reasons for why there is discrimination or stigma against the disease so he could address that in a more concrete way.

The Ministry of Education has agreed to introduce sex education and HIV-AIDS education into the curricula of the school system for the secondary and tertiary institutes. Also, to introduce HIV prevention education information about protection in adult literacy programmes.

The Minister of Health was also forthcoming to learn from other experiences in other countries and this year we will have a meeting of low prevalence countries in Manila and he's agreed to attend that, so he can learn from the experience of other countries.

I also met with Bishop Ricardo and that they will also do a lot more to speak out about stigma and discrimination and that they will introduce education for young people.

The civil society groups are quite active and there many organisations but they are still small programmes and they need more assistance and they need to be scaled up in to national programmes. They have some problems with access to condoms, and distribution systems, and access to their clients, so there are some issues that need to be resolved and these were identified.

And last, but not least, I want to recognise the very important UN system programme which is well coordinated and can lead by example. It is something that the Government could learn from. I have been to many countries and not all UN systems work together as one as it does in Timor-Leste. I want to specially recognise that and say that you are fortunate to have the leadership of this UN senior leadership. You can learn from them and they can learn from you and I would like to recognise my colleagues in this country.

Spokesperson. Does anybody have any questions?

Mr Khare, what can you tell us about the incident yesterday between the ISF patrol and as I understand it, the group of Major Alfredo Reinado.

We have received information that yesterday when the ISF patrol, near Lauala village in the Ermera District, was moving in that area there was some members of Alfredo Redinado's group who fired shots in the air. ISF has also confirmed to us that they did not fire any shot in return. No injuries have been reported. However, incidents of this type again bring me to the point that I have been saying from the very beginning.

It is extremely important that progress be made in the efforts to bring Alfredo Reinado to justice in a peaceful manner. And these efforts depend on the efforts of the Government and of Alfredo Reinado and his supporters.

And today, through you I want to call again on Alfredo Reinado, if he feels for this country, if he has the best interests of this country at heart to submit to justice in a peaceful manner.

UNMIT of course has a mandate to assist the country in the maintenance of public security and stability. And I, I would be telling the Security Council, depending on the developments today and up until the 14th of Febuary, that at the current state, the current juncture, the Government's efforts which are designed to bring Alfredo Reinado to justice in a peaceful manner should be supported.

I want to be very clear because there are many people who talk about solving the Reinado problem and I think that is a different question and not a question that I have asked at any time.

For me, to ensure the strengthening or rule of law and security in this country, the question has always been how to bring Alfredo Reinado to justice in a peaceful manner, which is a different question.

A question for Dr Sadik what are the efforts that have been made to deal with HIV-AIDS in Timor-Leste?

I think the country has done many things. It has a national strategic plan, it has a national aids commission, it has an active programme which is now being funded by the Global Fund and also Government funding It has four areas. One is the prevention and education of the high risk groups, mapping of high risk groups, providing education and services and access to treatment and care which is anti-retroviral treatment for those infected.

Also a number of civil society and NGO groups have been enabled to provide education and services to the high risk groups and they are doing very good work on accessing these people, looking after them and educating them.

Again to Mr Khare, there was, as I understand it, an explosion last night in the compound where the cantonment of the Petitioners will take place. Those two incidents with the ISF and Reinado in the same, what message will give to the Security Council in New York about the security situation.

The explosion was not in the compound. The explosion was on the road. As a result there is a certain portion of the road which has been affected which is about 15 feet.

PNTL, under the guidance of UNPol have begun forensic investigations. Of course yesterday as soon as the incident happened at 22.10 the PNTL task force immediately reacted and went there and remained there for about two hours. But there were no suspects, because despite arriving within 10 minutes, those who caused the explosion had left.

Through the media, I would like to appeal to the people of Timo-Leste that anybody with information who can assist in the investigation should provide the information to the police.

Coming to the report to the Security Council as you people have known me, I do not change positions on individual incidents. I still look at the broad picture. And looking at the broad picture I think that there is relative stability, but looking at individual cases I see that the security is fragile and which is why I strongly report the recommendations that the Secretary General has made to the Security Council that the UNMIT mission should be extended by one year.

I would like to ask about the letter that has been sent by FERTILIN to the SG on how to solve the Reinado case.

As you know every week I meet with the Prime Minister and the President. And regularly I meet with the leaders of political parties. After the announcement of the AMP government, as you remember the Political Party Accord clearly stated that those parties that form the Government will construct a meaningful role for the opposition.

Immediately in August I said I would have regular meetings with Mari Alkatiri as the Secretary-General of Fretilin and also the leader of the Opposition. Of course he does not agree to be the leader of the opposition, so I say every Wednesday the SRSG meets with the leader of the largest party outside of the Government. It just takes more words to describe the same thing.

So as you can see I am always in favour of this integral idea of democracy, that is, inclusiveness and broad based participation in decision making.

Ability to develop a consensus- or in the absence of consensus - to have compromised solutions is essential And therefore it is of critical importance that all parties in Timor-Leste must have the ability, that despite partisan differences, tost focus on solving the immediate problems, the Petitioners, the IDPs and how to bring Alfredo Reinado to justice in a peaceful manner.

All the parties have a responsibility to respond to that. And I am very happy to tell you that President Ramos-Horta, President of the Parliament Lasama , the Prime Minister Xanana Gusmão, and the leader of the Opposition Mari Alkatiri, all of them have agreed with me on this issue. A

I hope that with the efforts of President Ramos-Horta, who is the symbol and the guarantor of the sovereignty of this country, there will be positive results to the report to the Security Council by the Timorese authorities themselves.

It also important that apart from solving the immediate problems, parties and differences have to be set aside to promote the national interest. And these national interests immediately are related to the review of the security sector, the strengthening of the rule of law, promoting socio-economic development and promoting a culture of democratic governance. And I can inform you that in the first area, the review of the security sector reform a working group between FRETILIN and UNMIT has been established and it will meet every two weeks to take into account FRETILIN's opinion.

Yesterday's incident between Reinado and ISF, do you think it is necessary to set the limit of movement not to encroach in to Rienado's area?

The ISF is a legal force which is here upon the request of Timorese authorities to assist the Timorese authorities and to assist the UN. If any limit has to be placed, it has to be placed on the fugitive, which is Reinado. And this limit is what is known as cantonment and it is what the Government is trying to discuss and agree upon with Reinado.

From Alma Ata to the Global Fund: The History of International Health

2008-02-17T21:52:00.000-08:00

http://journals.sfu.ca/socialmedicine/index.php/socialmedicine/article
/download/\186/380

Italian Global Health Watch (OISG). Gavino Maciocco, President
Italian Global Health, Bologna, Italy. Social Medicine - Volume 3,
Number 1, January, 2008

"….Global Funds are like stars in the sky, you can see them, admire
them, appreciate their abundance… but fail to touch them…." Ministry
of Health Official, Malawi

Abstract: This paper traces the evolution of international health
policies and international health institutions, starting from the
birth of the World Health Organization, the setting up of the Health
for All target at the Alma Ata conference in 1978 and the rise of neo-
liberal policies promoted by international financial institutions
from 1980 to the present. The paper looks at different issues
surrounding public-private partnerships and the setting up of the
Global Fund to fight AIDS, Tuberculosis and Malaria and the influence
of these institutions on the health systems in poor countries.

Conclusions
The overview of the last sixty years of international health policy
presented in this paper results in the uncomfortable impression of a
substantial shift from a publicly funded, comprehensive system
approach to ensuring the right of health for all (enshrined in the
Alma Ata Declaration) to a privately-influenced, segmented, "just-for-
some" provision of health care goods and services typified by the
work of the Global Fund to Fight AIDS, Tuberculosis and Malaria.
Although it has been promoted as a foundation -- not a U.N. agency or
a broader development agency – and as such acting primarily as a
financing mechanism, rather than an implementing agency, the Global
Fund "works in cooperation with other groups -- multilateral
organizations, bilateral agencies, NGOS, civil society and faith
based groups -- that help design programs, provide technical
assistance, and otherwise provide support for country programs."30
As such the Global Fund has been and still is very influential in
shaping major international health policy choices that
warrant serious scrutiny from the global health community.

The Global Fund's failures described in this paper may be summarized
in the limited resources provided as compared to the Fund's declared
ambitions, its disappointing results (e.g. in terms of treatment
coverage) and its wider harmful consequences due, for instance, to
the competitive recruitment of staff in privileged areas of
intervention and consequent neglect of other sectors.

As these "collateral effects" have long been described since the
earliest debate on comprehensive as opposed to selective Primary
Health Care in the `80s, the Global Fund story represents in our
opinion a further example of how difficult it is to learn from
history, that is to aim at an evidence- based international health
policy. No health system in the world is actually built on "vertical"
programs. Nonetheless because of the GF an unduly strict selective
approach to health care delivery has often been introduced into poor
countries in the early stages of their development; this has had
destructive effects on their health systems, as even the IMF itself
has been forced to admit. In this world-view, a false distinction has
been perpetuated whereby the legitimate exercise of setting
priorities among competing needs has been translated into rigid, self-
contained programs that have often jeopardized local health systems.

As it is clear that the different financing mechanisms that support
international health policy choices have inevitably a substantial
bearing on health outcomes, it is imperative that those mechanisms
are adopted that are designed to:

Ensure universal access to basic health care, giving absolute
priority to the poorest and most vulnerable groups in the population
(children and women);

Reinforce whole health systems, instead of basing strategies on
vertical programs;

Strengthen infrastructures, organization and control of programs,
purchase and distribution of essential medicines (including
antiretroviral drugs for the treatment of AIDS);

And, above all, invest in human resources within the public health
sector through training, motivation, appropriate and just remuneration
of health personnel that will help block the drain of staff to the private
sector and abroad.

Science & Medicine | Studies Examine 'Creative' Uses of Antiretrovirals Aimed at Preventing HIV Transmission, San Francisco Chronicle Reports

2008-02-08T19:53:00.000-08:00

http://www.kaisernetwork.org/daily_reports/rep_index.cfm?DR_ID=50301

[Feb 08, 2008]

Researchers attending the 15th Conference on Retroviruses and Opportunistic Infections in Boston this week "could take heart" in several studies that found that "creative" uses of antiretroviral drugs might prevent transmission of the virus, the San Francisco Chronicle reports.

One study released at the conference that was conducted by CDC in Uganda during a three-year period found that the risk of HIV transmission decreased by 90% among discordant married couples -- in which one person is HIV-positive and the other is HIV-negative -- if the HIV-positive person took antiretrovirals. According to the Chronicle, the study's findings support the theory that the risk of transmitting HIV decreases among HIV-positive people taking antiretrovirals because their viral loads decrease. The purpose of the study was to determine whether potentially risky sexual behaviors increased among discordant couples if the HIV-positive person was taking antiretrovirals. The study found that the risk of unprotected sex did increase slightly but that antiretrovirals provided significant protection against HIV transmission. One HIV-negative spouse contracted the virus during the study.

Another study released at the conference conducted in rural Uganda found that an HIV testing program that utilized volunteers to conduct door-to-door testing "radically" increased the number of couples who received an HIV test. Almost 80% of the 220,000 people offered an HIV test during the study received one, and 4% were found to be HIV-positive. In addition, the study found 866 discordant couples. According to the Chronicle, earlier studies have found that risky sex decreases by 80% when discordant couples learn their HIV status.

In addition, another study released at the conference found that HIV-positive women who take antiretrovirals at the end of pregnancy and for six months after their infants' births while breastfeeding decrease the risk of vertical transmission. However, the study did raise a concern of future drug resistance among the women if they were not ill enough to need antiretrovirals while they were pregnant or breastfeeding, the Chronicle reports (Russell, San Francisco Chronicle, 2/7).

USA: No evidence that being circumcised was protective against HIV

2008-01-23T01:12:00.000-08:00

UNITED STATES: "Circumcision Status and HIV Infection Among Black
and Latino Men Who Have Sex with Men in Three US Cities"

2007 National HIV Prevention Conference Abstract Book Presentation number C01-4; P. 19-20 (12..07):: G.A. Millett; H. Ding; J. Lauby; S. Flores; A. Stueve; T. Bingham; A. Carballo-Dieguez; C. Murrill; K. Liu; D. Wheeler; A. Liau; G. Marks

The researchers undertook the current study to "examine characteristics of circumcised and uncircumcised black and Latino men who have sex with men (MSM) in the United States and assess the association between circumcision and HIV infection."

In New York City, Philadelphia, and Los Angeles, respondent driven sampling was used to recruit 1,154 black MSM and 1,091 Latino MSM. The researchers administered a 45-minute computer-assisted interview and a rapid-result oral fluid HIV antibody test (manufactured by
OraSure Technologies Inc.).

Seventy-four percent of the black MSM were circumcised, compared to 33 percent of the Latino MSM (P<.0001). In both racial/ethnic groups, circumcised MSM were more likely than those uncircumcised to be born in the United States or to have a US-born parent.

The authors found that circumcision status was not associated with prevalent HIV infection among Latino MSM, black MSM, black bisexual males, or black or Latino men who reported testing HIV-negative at their last test. Circumcision was found not to be associated with a
reduced likelihood of HIV infection among men who engaged in unprotected insertive anal sex and not unprotected receptive anal sex.

"In these cross-sectional data, there was no evidence that being circumcised was protective against HIV infection among black MSM or Latino MSM," the authors concluded.

CDC HIV/Hepatitis/STD/TB Prevention News Update 12/05/2007

The US FDA to revise blood donor criteria. An impetus for Asian countries to

2008-01-20T03:25:00.000-08:00

Published on AIDS-ASIA mailing list on December17,2007

Joe Thomas

(AAeF) The US Food and Drug Administration (FDA) proposes to revise and update
the regulations applicable to blood and blood components, including Source
Plasma and Source Leukocytes, to add donor requirements that are consistent with
current practices in the blood industry, and to more closely align the
regulations with current FDA recommendations. Perhaps, the blood transfusion
systems in various Asian countries should take the cue from the FDA's move and
take additional steps to ensure blood safety.

In many Asian countries blood transfusion system is inadequate to ensures the
safety of the donors and the recipients. In the 1990s, hundreds of thousands of
Chinese villagers were infected with HIV through state-run blood collection
centers. A blood safety scandal in Japan forced them to enact a blood law and
amendments in the Pharmaceutical Affairs Law were enforced in 2003 for the
purpose of securing a stable supply of blood based on domestic voluntary
donations and promoting the appropriate use.

1,872 haemophiliacs in Japan were infected with HIV, through transfusion of
contaminated blood and blood products.

About 11%of the male respondents from Hong Kong blood donations centres have
practiced `deferrable risk behaviours' (e.g sharing syringes, commercial sex
networking, or having sex with another man)Lau, Thomas and Lin 2002).

The prevailing severity of stigma and discrimination associated with HIV
infection may be the reason for many to use the blood transfusion centres
discreetly, rather than using HIV testing centres. Studies from Hong Kong and
Japan reported that people visit blood service centers for getting tested on HIV
infection instead of visiting VCT. (Sugimoto et al 2002,Lau, Thomas and Lin
2002)

FDA, believes that developing drastic exclusion criteria may help ensure the
safety of the national blood supply and to help protect donor health by
requiring establishments to evaluate donors for factors that may adversely
affect the safety, purity, and potency of
blood and blood components, or the health of a donor during the donation
process.

The FDA Notice of Proposed Rulemaking discusses the recommendations contained
in current guidance that fall under the proposed regulation, including donor
eligibility and screening for HIV and certain other transfusion-transmitted
infections.

According to FDA, the proposed rule will more explicitly describe donor
eligibility standards and will clarify the relationship between the regulations
and the applicable recommendations. The proposed rule, among other things,
provides for the establishment of minimum criteria for the assessment of donor
eligibility, and the suitability of the donation of blood and blood components.

The rule is expected to have a minor net impact on blood establishments because
it is already usual and customary business practice in the blood industry to
assess donors for eligibility, and donations for suitability. FDA believes the
primary impact of the rule will be the one-time review of current SOPs that the
proposed rule would require each blood collecting establishment to conduct.

FDA is suggesting the blood collection establishments to determine whether a
donor has engaged in social behaviors associated with increased risk of
infection with relevant transfusion-transmitted infections. According to the FDA
good guidance practices
participation in social behaviors associated with relevant
transfusion-transmitted infections would cause the donor to be ineligible to
donate and to be deferred.

Some examples of social behaviors associated with increased risk of exposure to
HIV and viral hepatitis identified in current guidance are men who have had sex
with another man even one time since 1977; exchanging sex for drugs or money; or
intravenous drug use. FDA included assessment of certain social behaviors
because of the risk that testing alone would not detect infection due to testing
error, the early stage of the donor's infection (the window period), or the
donor's low antibody level or intermittent viremia.

Notes and References:

Written or electronic comments on the proposed rule, may be submitted to the
agency until February 6, 2008
http://frwebgate.access.gpo.gov/cgi-bin/leaving.cgi?from=leavingFR.html&log=link\
log&to=http://www.regulations.gov.

Written submissions could be send by FAX: 301-827-6870. Or by mail/Hand
delivery/Courier to Food and Drug Administration, 5630 Fishers Lane, rm. 1061,
Rockville, MD 20852.

U.S. Food & Drug Administration (FDA). http://www.fda.gov/
(http://www.fda.gov/cber/rules/reqbldtrans.htm)

Sugimoto K, Takanishi Y, Nakaishi T, Kimura K, Imai M. Donor select for blood
safety from HIV contamination. Int Conf AIDS. 2002 Jul 7- 12; 14: abstract no.
MoPeD3672.

Lau JT, Thomas J, Lin CK. HIV- related behaviours among voluntary blood donors
in Hong Kong. AIDS Care 2002; 14: 481-49

Ten myths and one truth about generalised HIV epidemics

2007-12-29T22:45:00.000-08:00

James D Shelton a

The Lancet 2007; 370:1809-1811. DOI:10.1016/S0140-6736(07)61755-3

Despite substantial progress against AIDS worldwide, we are still
losing ground. The number of new infections continues to dwarf the
numbers who start antiretroviral therapy in developing countries.1,2
Most infections occur in widespread or generalised epidemics in
heterosexuals in just a few countries in southern and eastern Africa.
Although HIV incidence has fallen in Uganda, Kenya, and Zimbabwe, the
generalised epidemic rages on. Something is not working. Ten
misconceptions impede prevention.

HIV spreads like wildfire—Typically it does not. HIV is very
infectious in the first weeks when virus levels are high,3 but not in
the subsequent many-year quiescent phase. Only about 8% of people
whose primary heterosexual partners have the virus become infected
each year.4 Thus Kenya has more couples in which only one person is
infected than couples in which both are (figure).5 This low
infectiousness in heterosexual relationships partly explains why HIV
has spared most of the world's populations. However, the exceptional
generalised epidemics in Africa seem largely driven by concurrent
partnerships, in which some people have more than one regular
partner. This pattern allows rapid dissemination when a new infection
is introduced6 and probably involves more frequent risky sex than in
sporadic or exclusive relationships.

Sex work is the problem—Formal sex work is uncommon in these
generalised epidemics. In Lesotho, fewer than 2% of men reported
paying for sex in the previous year, although 29% reported multiple
partners.7 Nuanced economic support is an important enabler of
regular concurrent partnerships and transactional sex, but the
targeting of sex work in prevention campaigns has limited usefulness.

Men are the problem—The behaviour of men, including cross-
generational and coercive sex, contributes substantially to the
establishment of generalised epidemics. But a heterosexual epidemic
requires some women to have multiple partners.3 The importance of
women in generalised epidemics is evidenced by the high proportion
(sometimes the majority) of discordant couples in which the woman,
not the man, is HIV positive (figure).5

Adolescents are the problem—Generalised epidemics span all
reproductive ages. Although adolescent women are affected through sex
with older men, HIV incidence increases in women in their 20s and
later in life.8 Men are infected at even older ages. Thus
interventions in young people, including abstinence, although
important, have limited usefulness.

Poverty and discrimination are the problem—These factors can surely
engender risky sex. But HIV is paradoxically more common in wealthier
people than in poorer people, perhaps because wealth and mobility
support concurrent sexual partnerships.9 Moreover, HIV has declined
without major improvements in poverty and discrimination, notably in
Zimbabwe (notwithstanding substantial economic and social distress).
Condoms are the answer—Condom use, especially by sex workers, is
crucial to the containment of concentrated epidemics, and condoms
help to protect some individuals. But condoms alone have limited
impact in generalised epidemics. Many people dislike using them
(especially in regular relationships), protection is imperfect, use
is often irregular, and condoms seem to foster disinhibition, in
which people engage in risky sex either with condoms or with the
intention of using condoms.8

HIV testing is the answer—That learning one's HIV status (hopefully
with counselling) should lead to behavioural change and reduced risk
seems intuitive. However, real-world evidence of such change is
discouraging, especially for the large majority who test negative.3
Moreover any changes must be sustained for years. And very newly
infected people, who are highly infectious, do not yet test HIV-
positive.

Treatment is the answer—Theoretically, treatment and counselling
might aid prevention by lowering viral levels (and infectiousness) in
those treated, reducing denial about HIV, and promoting behavioural
change. However, no clear effect has emerged. Indeed these salutary
effects might be outweighed by negative effects, such as resumption
of sexual activity once those on antiretrovirals feel well, and
disinhibition when people realise that HIV might no longer be a death
sentence.

New technology is the answer—Many resources are devoted to vaccines,
microbicides, and prophylactic antiretrovirals. Unfortunately any
success appears to be far off. Moreover, such innovations might be
mainly targeted only at very high-risk populations, rely on
behavioural compliance, and engender disinhibition.10 Similarly,
treatment of sexually transmitted infections to prevent HIV has been
disappointing.11 Even male circumcision, an already available,
unmistakably effective, and compelling priority will take years to
have additional substantial effect.

Sexual behaviour will not change—Actually, facing the prospect of
deadly illness, many people will change. Homosexual men in the USA
radically changed behaviour in the 1980s. And the reductions in HIV
incidence in Kenya and eastern Zimbabwe were accompanied by large
drops in multiple partners,8,12 probably largely as a spontaneous
reaction to fear.

Truthfully, our priority must be on the key driver of generalised
epidemics—concurrent partnerships. Although many people sense that
multiple partners are risky, they do not realise the particular risk
of concurrent partnerships. Indeed, technical appreciation of their
role is recent.6 But partner limitation has also been neglected
because of the culture wars between advocates of condoms and
advocates of abstinence, because it smacks of moralising, because
mass behavioural change is alien to most medical professionals, and
because of the competing priorities of HIV programmes.

Fortunately we can enhance partner-limitation behaviour, akin to the
behaviour change that many people have adopted spontaneously. State-
of-the-art behaviour-change techniques, including explicit messages,
that are sensitive to local cultures, can raise perception of
personalised risk. Even modest reductions in concurrent partnerships
could substantially dampen the epidemic dynamic. Other prevention
approaches also have merit, but they can be much more effective in
conjunction with partner-limitation. Now, more than 20 years into HIV
prevention, we have to get it right.

I thank Daniel Halperin and Willard Cates for helpful ideas on this
Comment. My views here are not necessarily those of USAID. I declare
that I have no conflict of interest.

References

1. UNAIDS, WHO. AIDS epidemic update. December, 2007:
http://data.unaids.org/pub/EPISlides/2007/2007_epiupdat...
(accessed Nov 21, 2007)..

2. World Health Organization, UNAIDS, UNICEF. Towards universal
access: scaling up priority HIV/AIDS interventions in the health
sector. Progress report, April 2007. April 17, 2007:
http://www.who.int/hiv/mediacentre/univeral_access_prog...
(accessed Nov 21, 2007)..

3. Cassell MM, Surdo A. Testing the limits of case finding for HIV
prevention. Lancet Infect Dis 2007; 7: 491-495.

4. Wawer MJ, Gray RH, Sewankambo NK, et al. Rates of HIV-1
transmission per coital act by stage of HIV-1 infection, in Rakai,
Uganda. J Infect Dis 2005; 191: 1403-1409.

5. Central Bureau of Statistics, Ministry of Health Kenya, Kenya
Medical Research Institute, Centers for Disease Control and
Prevention Kenya, ORC Macro. Kenya demographic and health survey
2003. 2004:
http://www.measuredhs.com/pubs/pub_details.cfm?ID=462&c...
(accessed Nov 21, 2007)..

6. Halperin D, Epstein H. Concurrent sexual partnerships help to
explain Africa's high level of HIV prevalence: implications for
Pevention. Lancet 2004; 364: 4-6.

7. Ministry of Health and Social Welfare Lesotho, Bureau of
Statistics Lesotho, ORC Macro. Lesotho demographic and health survey
2004. 2005:
http://www.measuredhs.com/aboutsurveys/search/metadata....
(accessed Nov 21, 2007).

8. Shelton JD. Confessions of a condom lover. Lancet 2006; 368: 1947-
1949.

9. Shelton JD, Cassell MM, Adetunji J. Is poverty or wealth at the
root of HIV?. Lancet 2005; 366: 1057-1058.

10. Imrie J, Elford J, Kippax S, Hart G. Biomedical HIV prevention—
and social science. Lancet 2007; 370: 10-11.

11. Gray RH, Wawer MJ. Randomized trials of HIV prevention. Lancet
2007; 370: 200-201.

12. Gregson S, Garnett GP, Nyamukapa CA, et al. HIV decline
associated with behavior change in eastern Zimbabwe. Science 2006;
311: 664-666.

Affiliations

a. Bureau for Global Health, US Agency for International Development,
Washington, DC 20523, USA

Post-exposure HIV drugs won't boost risky behavior

2007-12-08T22:21:00.000-08:00

Fri Nov 23, 2007 12:11pm EST
By Anne Harding

NEW YORK (Reuters Health) - Giving antiretroviral drugs to people after they may have been exposed to HIV is an effective way to prevent them from contracting the virus, a new study shows.

What's more, people who know this option is available to them don't appear to be more likely to engage in risky behavior, Dr. Steve Shoptaw of the UCLA Department of Family Medicine in Los Angeles, who was involved in the research, told Reuters Health. "This is a viable way of helping people stay (HIV)-negative, " he said.

So-called post-exposure prophylaxis, or PEP, has long been available to people who risk HIV infection on the job, for example a health care worker accidentally jabbed by a contaminated syringe. In 2005, the Centers for Disease Control and Prevention expanded its PEP guidelines to cover people exposed to HIV outside the workplace, for example through risky sex, condom breakage or drug use. But PEP still isn't widely used in such cases, Shoptaw and his team note, because it isn't covered by health insurance and is only very rarely offered as part of community health programs.

To investigate the feasibility of a community organized and funded non-occupational PEP program, the researchers conducted a demonstration project in which people were offered a 28-day course of anti-HIV drugs within 72 hours of potential exposure to HIV.

One hundred people, 95 of them men, participated. They received the drug treatment, HIV testing, and counseling for up to 26 weeks after enrolling in the study. Fifty-eight participants reported having unprotected anal sex, while 18 percent reported condom breakage.
Among the 84 people given the full course of medication, 75 percent actually took all the drugs. No one became HIV-positive during the course of the study.

Some health authorities have been reluctant to offer PEP after risky sex or drug use for fear that people wouldn't change their behavior if they knew "there's a parachute somewhere they can take to stay negative," Shoptaw noted. However, he and his colleagues found people reduced their risk behavior after using PEP, rather than increasing it.

He and his colleagues call for making non-occupational PEP programs more widely available to people at high risk of becoming infected with HIV. For now, Shoptaw noted, PEP is available only to people who can access it and pay for it out of pocket -- drugs and counseling together cost about $2,200.

Right now, "this is more of a social justice issue," Shoptaw said. "People who have means have access to this, people who don't, don't."

SOURCE: AIDS Care, published online October 24, 2007.

© Reuters 2006. All rights reserved.

Deputy governor unwavering on plan to legalize prostitution

2007-12-08T22:20:00.000-08:00

Friday, November 23, 2007

Prodita Sabarini, The Jakarta Post, Denpasar

Bali Deputy Governor Alit Kesuma Kelakan has said he will push ahead
with plans to recognize and provide support to prostitutes in an attempt
to halt the spread of HIV/AIDS on the island, despite objections from
Governor Dewa Made Beratha.

Kelakan's plan involves declaring known prostitution zones safe from
persecution in order to encourage the women to access health services.
"Approved or not, I will go ahead with the program," Kelakan said.
Kelakan, who is chairman of the Bali chapter of the National AIDS
Commission (KPAD Bali), said he believed such policy a would enable
health-related agencies to better identify and reach HIV/AIDS high-risk
groups to curb the spread of the virus through sexual contact.

KPAD Bali data show that more than half of the island's HIV/AIDS
patients were infected with the virus through sexual contact.
According to the Kerti Praja Foundation, an organization working on
HIV/AIDS prevention in the island, Bali has around 8,800 sex workers
with a customer base of around 85,000.

Research by the foundation in 2006 also found that 14 percent of sex
workers in Bali are infected with the virus.

In a plenary meeting with the Bali Regional Legislative Council earlier
this month, Beratha firmly rejected Kelakan's proposal. He said that the
policy of acknowledging and accepting the prostitution areas would
suggest that the practice of prostitution has been legalized.
He said this was clearly in opposition to Bali's religious teachings,
customs and culture.

The Indonesian Criminal Code states that prostitution is illegal.
However, commercial sex workers are common in tourist areas of Bali such
as Sanur and Kuta.

Kelakan has said that law enforcement has been ineffective in stopping
the practice, which stems from more complex issues of poverty, poor
education and unemployment.

He policy suggestion has also met with resistance from legislators and
the Indonesian Hindu Council. The Council of Customary Villages
initially objected to the plan but later accepted it.

Kelakan said that KPAD Bali will carry out strict supervision programs
at known prostitution areas in a number of regencies, including the
regular monitoring of sex workers' health.

"KPAD and other non-governmental organizations have already carried out
campaign programs for sex workers, so without the government
implementing the program in its budget, KPAD's and the NGOs' programs
would still go on. However, it would only be partial (in its coverage
and impact). It would not be a systemized program and would certainly
not be a sustainable one. What we need is a sustainable program
supported by the government," he said.

Kelakan said that positive developments had been seen in Badung regency,
where the government and local council there were deliberating a bill on
HIV/AIDS prevention that would make it mandatory for owners of
entertainment places to educate their employees on HIV/AIDS and to
routinely check their employees' health status in relation to sexually
transmitted disease.

KPAD has estimated that the number of people living with HIV/AIDS on the
island exceed 4,000 as of August this year.

Head of Kerti Praja Nyoman Wirawan gave the "very conservative"
estimation that 840 men in Bali will contract the virus this year
through sexual contact with HIV-positive sex workers, with the
assumption that there are only 3,000 sex workers in Bali, with one
customer per day, working 250 days per year.

The estimate doesn't account for other potential infected people, such
as the sexual partners of customers and the babies of pregnant
HIV-positive- mothers.

"Imagine Bali in 10 to 20 years. If we don't do anything there will be a
lost generation of Balinese due to HIV/AIDS. The government is nothing
but a hypocrite if it does not try to do anything about this," he said.

Stephen Lewis damns UNAIDS over statistics revision; diverts from the

2007-12-08T22:06:00.001-08:00

Rob Dawson, Thursday, November 29, 2007

In a passionate speech at the World Health Editors Network in London,
a former United Nations Special Envoy for AIDS in Africa and
Co-Director of AIDS-Free World, Stephen Lewis, warned that a recent
UNAIDS document reporting decreased HIV infections has "undermined
public confidence in the reliability of the figures, introducing
completely unnecessary levels of doubt, contention and confusion".
Describing the UN as "stubborn and sloppy", he expressed concern that
the report does nothing to convince the world that we are "billions
and billions of dollars behind, when it comes to funding all the
components of the pandemic, from orphans to second line drugs."

In its latest report, UNAIDS cut the number of infections worldwide to
about 32.7 million, down from its estimated 39.5 million in 2006.
Rather than a reduction based on decreased rates of infection, the new
figure was mainly due to fixing flawed statistics from previous reports.
The former data collection methods relied heavily on "sentinel-site
surveillance" which extrapolates data gathered at prenatal clinics.
An assumption was made that the rate of HIV in the general population
would be similar to the rate among pregnant women in urban clinics.
This year the UN attributed more of their calculations to national surveys
and blood-testing.

While it's good news that fewer people are infected than previously
thought, there was concern that the dramatic re-representation of the
figures would result in diverted resources from an epidemic still in
desperate need of funds.

"For years, knowledgeable epidemiologists have been telling the UN
that the figures were too high. They didn't whisper their criticisms:
they wrote books and articles," Lewis said. "But the UN chose a course
of delay and dithering. It can never admit that it's wrong. So finally,
and predictably, came the moment of truth: the result is an overall
prevalence rate that is lower by almost seven million than last year's
estimate."

Lewis also expressed anger that the report did not address the human
tragedy and focused too much on statistics.

"The new estimates confirm a continuing apocalypse for sub-Saharan
Africa: 22.5 million infections, 61% of them women, 68% of world-wide
infections, 76% of all deaths, 11.4 million orphans. This is where the
focus must be, this is where it should always have been; not a report
cluttered by mathematical adjustments so that virtually every story
that's written begins with the news of a statistical volte-face. If the
recording of data had been more scrupulous all along, we could have
welcomed this report," he said. "Instead, all of us have to run to the
trenches to remind the world that more money is still desperately needed."

Lewis also highlighted several flaws in the data which could lead to
yet another recalculation. For example, the narrative evidence of the
report states repeatedly that Mozambique has shown no decrease in
infection rates yet later asserts that Mozambique is one of the six
countries in the world that has most significantly contributed to the
reduced numbers seen in the report. No data on Mozambique is set out
conclusively in the report.

In conclusion, Lewis stressed that more should be done no matter what
statistical calculation is applied to the figures.

"Whether it's 40 million or 33 million, this plague continues to
ravage humankind. I simply do not believe that the United Nations has
done everything it can possibly do to turn the tide," he said.

AIDS denial in Asia: Dimensions and roots

2007-11-25T15:06:00.000-08:00

Health Policy, Volume 84, Issues 2-3, December 2007, Pages 133-141

Binod Nepal ,(nepalbinod@....
National Centre for Social and Economic Modelling, University of
Canberra, ACT 2601, Australia

Abstract
AIDS denial has long been viewed as the obstacle to forging effective
response in many Asian countries. This article examines the
dimensions and roots of this phenomenon. It identifies seven types of
views, attitudes, or tendencies that can be described as denial,
dissent, disagreements, or doubts.

Three major factors underlying the AIDS denial are discussed. These are (1)
historical impressions that STDs are Western diseases, (2) desire of some Asian
leaders to forge Eastern points of view, and (3) long-held negative image
towards the peoples or groups who happened to be at the front-line of the
population groups exposed to the epidemic. The third factor is the most
important source of denial.

AIDS denial is not a new and isolated phenomenon but the one shaped by the
global and historical institutions. Asian AIDS denial reflects the authoritarian
and moralist grievances arising from the perceived deterioration of traditional
moral order.

Fax: +61 2 6201 2751.

Health Policy. Volume 84, Issues 2-3, December 2007, Pages 133-141

doi:10.1016/j.healthpol.2007.04.011
Copyright © 2007 Elsevier Ireland Ltd All rights reserved.

UN slashes AIDS estimates to 33 million

2007-11-22T02:12:00.000-08:00

http://au.news.yahoo.com/071120/2/150ly.html#

Tuesday November 20, 03:12 PM

The United Nations has slashed its estimates of how many people are infected with the AIDS virus, from nearly 40 million to 33 million.

In a report, the UN says revised estimates on HIV in India account for a large part of the decrease.
The agency admitted it overestimated how many people were infected with the incurable virus, and said better methods of collecting data showed it was not quite a common as feared.

"The single biggest reason for this reduction was the intensive exercise to assess India's HIV epidemic, which resulted in a major revision of that country's estimates," the report said.

After originally estimating some 5.7 million people were infected in India, the UN more than halved that estimate, to 2.5 million.

But the numbers nonetheless show the epidemic is overwhelming and that efforts to fight HIV must still be stepped up, said officials at the UN AIDS agency UNAIDS.

"These improved data present us with a clearer picture of the AIDS epidemic, one that reveals both challenges and opportunities," UNAIDS Executive Director Dr Peter Piot said in a statement.

"Unquestionably, we are beginning to see a return on investment - new HIV infections and mortality are declining and the prevalence of HIV levelling. But with more than 6,800 new infections and over 5,700 deaths each day due to AIDS, we must expand our efforts in order to significantly reduce the impact of AIDS worldwide."

The new numbers suggest that some 33.2 million people are infected with the human immunodeficiency virus - about 30.8 million adults and 2.5 million children.

UNAIDS estimated that 1.7 million people became newly infected in sub-Saharan Africa this year, a significant reduction since 2001.

But Africa remains by far the continent hardest hit by AIDS, with 22.5 million people infected with HIV.
"Eight countries in this region now account for almost one-third of all new HIV infections and AIDS deaths globally," said UNAIDS.

"In Asia, the estimated number of people living with HIV in Vietnam has more than doubled between 2000 and 2005 and Indonesia has the fastest growing epidemic."

The report gives two reasons for the downward revisions - one is better data and the other is an actual decrease in the number of new infections.

"UNAIDS and (the World Health Organisation) are now working with better information from many more countries," UNAIDS said.

The number of new HIV infections each year likely peaked in the late 1990s at 3 million and was estimated at 2.5 million for 2007, UNAIDS said.

"This reflects natural trends in the epidemic, as well as the result of HIV prevention efforts. Of the total difference in the estimates published in 2006 and 2007, 70 per cent are due to changes in six countries: Angola, India, Kenya, Mozambique, Nigeria, and Zimbabwe," the report said.

"In both Kenya and Zimbabwe, there is increasing evidence that a proportion of the declines is due to a reduction of the number of new infections which is, in part due to a reduction in risky behaviours."

The UN also changed its estimate on how long it takes to die of AIDS if not treated from 9 years to 11 years.

Joint Statement of the Three Delegations in support of Civil Society's uniquerole in responding to HIV/TB/Malaria in ChinaKunming, China, 16 th Global

2007-11-13T20:21:00.000-08:00

November 12, 2007
Having had some extremely valuable formal and informal interactions with a range of China Civil Society and Communities representatives over the last 5 days, the Communities Delegation along with Developed and Developing Country NGOs Delegation would like to strongly recommend to the Global Fund Board that a special attention is given to the need for strengthening Civil Society involvement and participation in the implementation of GF programs in China.

As with all grants there will be challenges in implementation. In particular, in the case of China and the recently-approved round 6, community and grassroots organizations cannot register to be legally recognized as civil society organizations.

We expect that these grassroots organizations, registered or not, should have access to the funds so that the implementation efforts will reflect the desired goal of the proposed program.

We, the members of the three civil society delegations to the Fund feel responsible and accountable to ensure that our counterparts in China are alsoable to access and utilize the opportunities of being a stakeholder in the Global Fund.

We are committed to ensure that the voices and aspirations of all communities living with the diseases in China are heard and that their basic rights, particularly the right to information and services are properly secured.

We expect the Global Fund to take the lead in ensuring its commitment to strengthen capacity building and mobilization of Civil Society across the world, including China, so that our collective goal of containing and reversing the spread of HIV/TB/Malaria is achieved.

We, the three civil society delegations, will continue to proactively engage with Chinese civil society to ensure their key role in the response tothe three diseases is recognized and we will work in close collaboration withall of you until this is achieved.

Communities Delegation
Developed Countries NGO Delegation
Developing Countries NGO Delegation to the Global Fund Board
Published at AIDS-ASIA yahoogroups, Tuesday, November 13,2007

Interpol to fight sale of fake medicines in Africa

2007-11-13T20:03:00.000-08:00

http://health.yahoo.com/news/afp/policeinterpolafricacounterfeitme
dicinehealth-print.html

By AFP

International police body Interpol will join the fight against the
growing trade in Africa in fake drugs for tuberculosis, malaria and
HIV/AIDS which threatens the lives of thousands, a senior official
said Tuesday.(AFP/File/Issouf Sanogo)

MARRAKECH, Morocco (AFP) - International police body Interpol
will join the fight against the growing trade in Africa in fake drugs for
tuberculosis, malaria and HIV/AIDS which threatens the lives of
thousands, a senior official said Tuesday.

The agency's efforts will begin later this year and will build on its
success in tackling the problem in Latin America and Southeast Asia,
said John Newton, the manager of Interpol's intellectual property
rights project.

"We have learned a lot of lessons in those regions and we are now
able to apply those to Africa," he told AFP on the sidelines of
Interpol's annual general assembly in Marrakech in southern Morocco.

Congo, Nigeria, Senegal and Sudan asked the 186-member police
body at the gathering for for help in stopping smuggling networks
from making fake drugs readily available in their markets and
sometimes even pharmacies, he said.

"The Africans are very keen for Interpol to work with them on this
subject," said Newton.

Interpol will train police in Africa on how to smash counterfeit
medicine smuggling networks, coordinate police operations and track
the flow of fake drugs from southeast Asia and other parts of the
world to the continent.

As it has in other regions, the global police body will work with the
World Health Organization and drug companies to tackle the problem.

"We can bridge the gap between law enforcement and the public
health sector, we are able to bring the two areas together," said Newton.

The World Health Organization estimates that up to 30 percent of the
medicine sold in Africa is fake.

Counterfeit medicine networks take advantage of Africa's poor or
non-existent drug regulatory systems to dump drugs with little or no
active ingredient in the continent, experts say.

Interpol carried out its first-ever operation solely dedicated to the
trade in fake medicine in 2005 in seven southeast Asian countries.

"We are concerned about counterfeit medicines for life-threatening
diseases such as malaria, tuberculosis and HIV/AIDS and increasingly
getting involved in this area," said Newton.

The US-based Center for Medicines in the Public Interest estimates
that global counterfeit drug sales will rise to 75 billion dollars by
2010, a 90 percent increase over 2005.

Russian scientists offer hope for HIV vaccine

2007-11-10T04:03:00.000-08:00

http://en.rian.ru/russia/20071005/82647847.html

NOVOSIBIRSK October 5 (RIA Novosti) - Scientists at the Russian virology and biotechnology Vector research centre in Novosibirsk, West Siberia have developed a potential HIV vaccine.

"As we know there is no HIV vaccine. The Americans had high hopes of developing one, but the three vaccines developed most recently all failed trials. Today the specialists from Vector said there is a hope for an effective vaccine," a leading geneticist, Vladimir Shumny, said on Friday.

The scientist added that it is difficult to develop an HIV vaccine as the virus is constantly mutating. He also said that the polymorphous vaccine created by the research center might help to effectively prevent HIV, however.

At the same time, Shumny claimed that lengthy legal procedures could complicate the vaccine's chances of passing the necessary medical trials, not to mention getting it registered with the appropriate authorities.

"The first phase of trials will take at least three years," he explained.

A researcher at Vektor added that it was still too early to speak about the effectiveness of the vaccine, as the first phase of the trials has not started and its safety has not yet been proven.

A total of 37 HIV vaccines have been developed, but none of them have been successful, she added.

The Russian government has allocated one billion rubles ($39.4 million) to develop a HIV vaccine.

Since 1987, when the first HIV case was first reported in Russia, 388,871 cases have been registered in the country, and HIV-infected women have given birth to 1,200 children. Among the most infected areas in Russia are Moscow, Irkutsk, Samara, Orenburg, and the Leningrad Region.

At the end of 2005, 40.3 million people were HIV-infected worldwide, including 17.5 million women and 2.3 million children under the age of 15.

Pre-treatment CD4 Count Predicts CD4 Gains on Treatment

2007-11-10T03:45:00.000-08:00

http://www.aidsmeds.com/articles/hiv_cd4_uk_1667_13356.shtml

October 30, 2007

By David Evans

The higher a person’s CD4 count upon starting HIV treatment, the higher their CD4 count will be 60 months later, say British researchers at the 11th European AIDS Conference in Madrid.

Rachael Hughes, MSc, of the department of social medicine at the University of Bristol in England, and her colleagues analyzed data involving 4,559 patients participating in the U.K. collaborative HIV Cohort (UK-CHIC), all of whom had maintained undetectable viral loads for at least six months after starting HIV treatment. Data were available for 631 patients who had been followed for greater than 60 months.

The research team found that CD4 gains were universally good among all of the patients in the study, regardless of their starting CD4 count. Those who started treatment with the lowest CD4 count, between 0 and 100, had the largest gains of up to 379 cells, while those who started with the highest, 500 and above, had the least gains, roughly 100 cells.

However, the average CD4 count 60 months after starting treatment was 100 cells lower among those who started treatment with CD4 counts between 350 and 499, compared with those who started with between 500 and 749 cells.

While these data suggest that people who start HIV treatment earlier will, on average, do better immunologically than those who start later, they also illustrate that almost all patients, regardless of their starting CD4 counts, can expect robust CD4 increases as a result of treatment. This research also concludes that CD4 gains are most noticeable during the first few months of treatment but do continue even after a year of treatment.

Source:

Hughes R, Sabin C, Sterne J. Long-term Trends in CD4 Count in Patients Starting HAART: UK-CHIC Study [Abstract P18.4/04] 11th European AIDS Conference, Madrid, 2007.

Early Treatment Reduces Risk of Three Common Complications

2007-11-10T03:31:00.000-08:00

http://www.aidsmeds.com/articles/kidney_neuropathy_anemia_1667_13376.shtml

November 2, 2007

Does starting HIV treatment early increase the risk of complications like peripheral neuropathy, anemia and kidney problems? On the contrary, say new data from the HIV Outpatient Study (HOPS) to be reported in an upcoming issue of the Journal of Acquired Immune Deficiency Syndromes (JAIDS).

Peripheral neuropathy, anemia and kidney problems are common occurrences in people with HIV, notably those on antiretroviral (ARV) treatment. In turn, some experts have suggested that starting treatment earlier than is currently recommended—a CD4 count below 350 cells—may result in an upswing in these complications among otherwise healthy people living with the virus.

The HOPS investigators, under the direction of Kenneth Lichtenstein, MD, of the University of Colorado in Denver followed 2,165 HIV-positive patients who started ARV treatment with varying CD4 counts for approximately three years. Patients were divided into three groups: those who started with CD4s below 200, between 200 and 349, and 350 or higher.

Among patients starting therapy with CD4s above 200, the number of new cases (incidence) of peripheral neuropathy, anemia and kidney problems—and the risk for these complications—was lower, compared with those starting HIV treatment with CD4s below 200. The incidence and risks of kidney problems were similar among those starting therapy with CD4s above 350 versus 200 to 349, but the risk of peripheral neuropathy and anemia was found to be lower among those starting with 350 or more CD4s.

Dr. Lichtenstein’s group also reported that the incidence of each condition decreased rapidly and remained low the longer patients remained on ARV therapy. The risk of these complications occurring was actually highest during the first three months of treatment, regardless of the pre-therapy CD4 count.

Assessing a Failed AIDS Vaccine

2007-11-10T00:21:00.000-08:00

After 20 years of defeat, it appeared that science may have finally developed a viable vaccine against AIDS. Merck's new drug, V520, was being tested in a huge clinical trial, involving 3,000 people in 15 cities, and it was widely considered the most promising new candidate in the field.

But last September, when Merck analyzed its initial trial data, it found that the vaccine had failed - and failed miserably. On Wednesday, the company issued its first report on the V520 trials, revealing that the drug did not protect against HIV, and more disturbingly, actually increased some people's susceptibility to the virus. "I don't think anyone imagined the results would be so definitively negative so quickly," says Dr. Gary Nabel, director of the Vaccine Research Center at the National Institutes of Health.

V520 may have failed, but somewhere in the details of the drug's nonsuccess, scientists hope to find insight into what will make future vaccines work. After all, V520 is just one of about 50 experimental HIV vaccines that are currently being tested in clinical trials, and almost all of them are designed to function the same way. While most vaccines expose the body to weakened or killed viruses, or pieces of them, to boost production of antibodies - proteins that recognize invading cells and flag them for destruction - that tack alone was too feeble to fend off HIV.

The new class of vaccines, including V520, takes a more direct route: They trigger cell-mediated immunity, which marshals killer T cells that both recognize and destroy viruses and bacteria, and can lead to a more robust, specific and longer-lived immune defense. It's not yet clear why V520 didn't work, but one theory involves its vector, or delivery vehicle. Like almost every other AIDS vaccine in development, Merck's drug used the common cold virus to transport its payload - three synthetic HIV genes - into the body's cells. What makes the adenovirus ideal for the task is precisely the reason colds make us so miserable - once inside a host, the cold virus infects cells and starts to replicate quickly.

The down side to that efficiency, however, is that cold viruses are so common that most people have developed a certain level of tolerance to them; if the adenovirus fails to excite the immune system, then any bugs piggybacked on the virus, such as HIV genes, will also slip past immune defenses. That's exactly what appears to have happened in the Merck trial: People with the highest pre-existing immunity to the common cold also had the highest rates of infection with HIV.

"It could be due to chance, or to differences in the populations we studied, or to something related to the vaccine itself," says Dr. Keith Gottesdiener, vice president of Vaccine and Infectious Disease Clinical Research at Merck. "The 'why' is still not well known.

" Researchers have already set about trying to figure it out. "We have to remember that Merck's was a single product testing a vaccine concept, which is that T cell immunity can protect against HIV infection," says Nabel. "And we know there are other ways to stimulate T cell immunity." Nabel is ready to test one such method, a vaccine similar to Merck's that uses different HIV genes and a "prime-boost" approach that involves two injections spaced a few months apart, instead of one shot, to maximize the stimulation of the body's T cells.

Other researchers, like Dr. David Ho, director of the Aaron Diamond AIDS Research Center in New York City and the recipient of a $25 million grant from the Gates Foundation to study novel vaccine strategies, think that the cold virus isn't the best way to deliver HIV. Ho is exploring the possibility that a different vector, such as the chicken pox virus, or perhaps no vector at all - simply injecting snippets of naked HIV DNA - could yield stronger immune responses.

At the International AIDS Vaccine Initiative (IAVI), a non-profit group of public and private partners focused on funding and accelerating AIDS vaccine research, scientists are studying the use of crippled, live strains of HIV - based on the success of other such live attenuated vaccines against polio and measles - which they think might be critical to waking up the right immune system defenses. "There is something magical about the replicating virus, because it has virtually its entire genome," says Dr. Seth Berkley, president of IAVI. His group is also investigating ways to stimulate so-called neutralizing antibodies, a special class of antibodies that appear to be able to defuse HIV.

Despite the ongoing study, experts argue that none of it will succeed without some basic changes in the way it's conducted. Most research occurs in isolation; there's little coordination among labs and no network through which data can be shared, making it difficult for scientists to learn from each other's missteps. Worse, it takes years to get regulatory approval to start a human trial for a new vaccine - not to mention enrolling the volunteers and training the right personnel - so, by the time experiments get underway, the science around which the vaccine was built has long since become outdated. "The trials are not informing science at the moment," says Dr. Alan Bernstein, executive director of the Global HIV Vaccine Enterprise, an alliance of independent organizations dedicated to accelerating HIV vaccine research. "Science - and vaccine development - is an iterative process, except that in HIV vaccine research, there isn't a lot of iteration going on."

The Enterprise, which was founded in 2005, intends to change that. With funding from the Gates Foundation, Wellcome Trust, National Institutes of Health and the European Union, it will serve as a hub for guiding worldwide HIV vaccine research. We want to ensure that the trials are done faster, better and smarter, says Bernstein. And hopefully, with more success. [TM]

Asian Diet: Nutrition key to surviving HIV/AIDS, WHO says

2007-10-31T05:06:00.000-07:00

Bangkok - Well-balanced meals are a key ingredient to survival forthe millions of HIV/AIDS patients in South and South-East Asia, WorldHealth Organization (WHO) experts said Tuesday.

"Nutrition and HIVare closely related," said Samlee Plianbangchang, WHO's regionaldirector for South-East Asia."HIV affects nutritional status, and poor nutrition in turn leads tofaster progression of HIV to AIDS," Samlee told a seminar of healthworkers and experts who gathered in Bangkok this week to findsolutions to fighting the two epidemics of malnutrition andHIV/AIDS. "Scaling-up care and antiretroviral therapy cannot beaddressed without appropriate support for nutrition.

"There are an estimated 4 million people suffering from HIV/AIDS inBangladesh, Bhutan, India, Indonesia, Nepal, Myanmar, Thailand, SouthKorea and Sri Lanka, the area defined by the UN agency as South-EastAsia.The good news is that most Asian diets are well-suited to providingthe nutrition HIV/AIDS patients require."I think Thai food is well-balanced and has all the nutrientssomebody needs, but it depends on keeping the right balance of carbohydrates, proteins and fats," said Ranga Saadeh, a scientist working for WHO's nutrition department in Geneva.Evidence has established that people living with HIV have higher energy needs than those who are HIV-negative.

Asymptomatic HIV-positive adults or children need 10 per cent more energy than those who are not HIV-positive, and those at advanced stages need 20 to 30 per cent more energy to maintain body weight,Saadeh said.HIV-positive children who are losing weight need 50 to 100 per centmore energy, she said. Providing a balanced, nutritious diet in countries where malnutritionis endemic poses an added challenge to their health services.

"This HIV/AIDs epidemic is being superimposed on the already existing malnutrition problems," Saddeh said, "so if we want to make a difference, we should really deal with both challenges at the sametime.

"http://www.earthtimes.org/articles/show/121064.html

"Impact of AIDS on children remains under-researched and poorly

2007-10-27T20:59:00.000-07:00

(Speech Check against Delivery) Dr Peter Piot UNAIDS Executive
Director's speech at the JOINT LEARNING INITIATIVE ON CHILDREN AND HIV/AIDS: International Symposium. Harvard Medical School. 24 September 2007.

I first want to thank Jim Kim, Peter Bell, Agnes Binagwaho for
inviting me here today, and to pay tribute to the tremendous work
they – and all of you – are doing. It is a privilege to be here today
with so many experts and activists. The issue of children and AIDS
was overlooked for far too long. UNAIDS was one of the first to
welcome the creation of the Joint Learning Initiative on Children and
AIDS, and I look forward to hearing about the progress you've made.

Let's start by looking at progress on AIDS in general. It's a mixed
picture, but there definitely is progress.

Today, 2.5 million people in developing countries are taking anti-
retroviral treatment up from 100,000 in 2001.

And in some populations in East Africa, the Caribbean, and Asia, HIV
infections are falling.

But if HIV is declining in some populations, it is rising in others.
In some Asian countries there's an upsurge in HIV infections among
men who have sex with men, but infections are declining in other
groups. The most striking overall increases have taken place in East
Asia, Eastern Europe, and Central Asia: the number of people
living with HIV went up by one fifth here between 2004 and 2006.

Globally, young people (15-24) accounted for 40% of new HIV
infections last year.

One in seven new HIV infections last year occurred among under-
fifteens. By the end of 2006, 2.3 million (1.7-3.5 million) children
(under 15) were living with HIV.

Let's just remind ourselves that the United Nations Convention on the
Rights of the Child defines children as people up to the age of 18.

But AIDS epidemiologists compile information for under fifteens and
for 15-24-year-olds. Lack of disaggregated data for children makes it
even harder to take effective action on their behalf.

One reason for this is the feminization of the epidemic: almost half
of all adults living with HIV are women. Only one in ten pregnant
women with HIV in low and middleincome countries receives anti-
retroviral prophylaxis to prevent transmission of HIV to their
children. Every year, more than 500,000 children are infected via
transmission from their mothers.

But this is just one way children become infected with HIV. Sexual
abuse is another.

The second (and main) way is through sex – whether it's between young
girls and older men, sex between adolescents, or sex between
trafficked girls or boys and clients, sexual violence and rape, or
incest.

A third cause of infection is injecting drug use, which often starts
in adolescence. In Russia, 76% of all people living with HIV are or
have been injecting drug users.

This is all fuelled by ignorance about HIV transmission. It's amazing
how prevalent this still is in 2007. I've just come back from China
where most young people have barely a clue about how HIV is
transmitted.

At the same time, only one in ten children needing HIV treatment can
get it – even though paediatric drug formulations are much more
widely available, and the price of antiretroviral drugs for children
has dropped – in some cases to less than 16 US cents per day. Just 4%
of children born to HIV-positive mothers receive cotrimoxazole, which
WHO recommends providing to children when early diagnosis of HIV
infection is unavailable. In Botswana and Zimbabwe, child mortality
rates have nearly doubled since 1990.

Last eek UNICEF reported some remarkable declines in child mortality
throughout the world, for the first time fewer than 10 million
children under five died – except in countries with high HIV
prevalence and those in conflict.

More than 15 million children worldwide have now been orphaned by
AIDS – over 12 million in Southern and East Africa. Orphan
populations are increasing in some populations in Asia, Latin America
and the Caribbean, and Eastern Europe too.

This much we know. Now let me turn to what we don't know.

We are constantly striving to know more about the AIDS epidemic,
through better and more accurate data collection. But there's still a
long way to go.

Today's surveillance categories are too broad and too blurred.
Collecting data for children up to the age of 15 and then for young
people between the ages of 15 and 24 doesn't give us the sort of
information we need: there's a huge difference in terms
of action between HIV infection at 15 and acquiring HIV at 24.

We need much more refined data about different age groups. We also
need to distinguish between the different categories of orphan –
"double", "one parent", maternal and paternal. And we need to become
much more systematic in pinpointing the differences between epidemics
within countries.

We also need to re-evaluate the way we perceive the issue of children
and AIDS. As so often happens, we have tended to only do this through
the medical lens, with a primary focus on mother to child
transmission. But this is to over-simplify, and to
ignore critical social and rights-related issues.

One problem is that we don't know enough about what these issues are.
We sense that AIDS is breaking up families and communities and
challenging traditional safety nets. We know that the impact on
household welfare is greater on the poor than on the better off, and
that gender inequities make girls more vulnerable than boys. We
are aware that it is threatening children's rights - civil,
political, economic, social and cultural.

And then there's the new reality: older children living with HIV. In
recent years, I've been meeting increasing numbers of HIV positive
adolescents and young adults.

But we often still lack hard, empirical data: the impact of AIDS on
children remains under-researched and poorly understood. We simply
don't know enough about what is happening. That's why the Joint
Learning Initiative is so badly needed.

Now let's look at what action is being taken today.

It's nearly 20 years since world leaders decided that people under 18
needed their own convention. That convention - the 1989 United
Nations Convention on the Rights of the Child, famously ratified by
all UN Member States except the US and Somalia – stresses the
importance of making the "best interests of the child" a
primary consideration and lists a series of rights. These include
such basics as information, education, non-discrimination, health,
social security, an appropriate standard of living, to be protected
from violence and different forms of exploitation, and the right not
to be separated from their parents. All are critical if children are
to grow up to live safe and healthy lives in a world with AIDS.

Since then, a series of international meetings and declarations have
highlighted the urgent need to address the issue of children and
AIDS. But to what extent are these declarations being acted on?

A few countries have substantially increased access to services to
prevent transmission of HIV from parents to children. For example, in
Argentina, Botswana, Jamaica, and Ukraine, more than 85% of HIV-
positive pregnant women received antiretroviral drugs to prevent
transmission of HIV to their children.

Some countries - including Botswana, Rwanda, and Thailand - have
scaled up HIV treatment for children by integrating it into treatment
sites for adults. Thailand is getting antiretrovirals to more than
95% of the under-15s in need.

Several countries in southern Africa have provided child grants and
other benefits on a national scale. Kenya, Malawi and Mozambique have
piloted cash-transfer programmes in poor areas.

In 58 countries surveyed last year, 74% of primary schools and 81% of
secondary schools said they were providing AIDS education. This is
critical if adolescents are to protect themselves from infection. To
be effective, AIDS education must fulfil the right to information (as
required in the Convention on the Rights of the Child). It must
provide information about all risks, and offer a broad palette of
prevention options – including abstinence, condoms, and measures to
address inequalities between girls and boys.

More efforts are being made to see that children get a fair share of
AIDS funding. A number of donors including the US and UK have
earmarked at least 10% of their AIDS money to go towards services
for children.

And lastly, more is being done to integrate services – to forge links
across diseases and sectors and bring partners closer together. In
Kenya, Rwanda, Tanzania and Zambia, strategic investment of AIDS
funding is improving services such as immunization and antenatal
care. And Norway's Women and Children First Initiative sets out to
provide a continuum of care for mothers, newborns, and children.

Many organizations are providing support to help countries look after
their children better. UNAIDS co-sponsor UNICEF, for example, has
made tackling children and AIDS one of its top priorities.

In 2005, UNAIDS joined UNICEF to launch "Unite For Children, Unite
Against AIDS", which sets targets for scaling up "The Four Ps":
prevention of HIV transmission from mother to child, paediatric
treatment for HIV, prevention of HIV among adolescents and young
people, and protection and support for children affected by HIV.

And as Peter mentioned earlier, civil society groups –the Elizabeth
Glaser Paediatric Foundation, the Ecumenical Advocacy Alliance and,
of course, the Francois-Xavier Bagnoud Association – are doing
tremendous work.

But most importantly of all, communities are responding and adapting
to the new realities around children and AIDS – often with tremendous
resilience.

So how do we build on this progress and intensify its impact?

We're here today because there are no simple answers to these
questions.

AIDS, as many of you have heard me say before, is an exceptional
issue – in terms of its threat to humanity and its complexity. The
Joint Learning Initiative was itself born out of recognition that the
issue of children and AIDS is immensely complex – and that it
requires a complex response.

I would like to suggest seven elements that I regard as key to making
that response effective.

First, it must be firmly grounded in human rights principles – in
line with the 2003 Comment on the Convention on the Rights of the
Child that "the child should be placed at the centre of the response
to the pandemic, and strategies should be adapted to children's
rights and needs". To be effective, those strategies have to
work equally well for seven-year-olds as seventeen-year-olds.

Second, it must involve a wide range of actors – not least the
children concerned, their parents, grandparents, and members of the
communities they live in. This means bringing children and family
members – including those living with HIV - to the table when
programmes are designed.

Third, it must prevent new HIV infections – for example by scaling up
access to services to prevent mother to child transmission and by
making HIV prevention more available and accessible to adolescents.
By addressing vulnerability and – though I know this is
controversial – by preventing sexual transmission. Universal Access to
HIV prevention, treatment, care and support is not only for adults!

Fourth, it must provide treatment for children. This will mean
scaling up testing and counseling, and making antiretroviral drugs
and cotrimoxazole more easily available.

Fifth, it must provide adequate levels of social welfare to children
infected and affected by HIV, and to their families and communities –
for example through cash transfers.

Sixth, it must be fully funded at international and national level.
This means more money for children and AIDS from international donors
and a higher priority for children in national development plans. At
UNAIDS, we estimate that $2.7 billion will be needed for programmes
for orphans and vulnerable children in 2008.

And finally, as I mentioned earlier, it must be based on more
accurate information.

This means not just improving surveillance but also clarifying how
children become vulnerable, looking more closely at socio-economic
contexts, and intensifying research into psychosocial impacts and
responses. It means looking at children in the contexts of their
families and communities, improving monitoring and evaluation
systems, studying how households cope and what local care-giving
practices involve.

To turn this wish-list into reality, high levels of political will
and commitment will be required. To inform and drive the process
forward, we will need a growing body of knowledge about children and
AIDS. We will need evidence from successful

interventions to show what can be done. And we will need sustained
activism to make sure the right action is taken – now and in the
years to come.

This brings me to my conclusion: it is time now to bite the bullet
and start thinking and acting in the context of the longer term –
something we have repeatedly failed to do up to now. Here, children
clearly have a major role to play.

We need to be confident that what we are doing now works on two
levels – both now and in the years to come. We must take steps now so
a girl born today doesn't grow up to produce an HIV positive baby and
so children born with HIV get anti-retroviral treatment and live
longer, healthier lives.

This means doing what you are doing in the Joint Initiative: taking a
long, hard look at what we are doing, identifying what works and
coming up with new approaches and new research to address new trends.

It means working together in a coherent fashion, on long-term,
integrated programmes: the day of the short-term, ad-hoc project is
over.

And it means ensuring that our response is comprehensive, flexible
and anticipatory - tailored to different epidemics and ready to
change as epidemics evolve: AIDS doesn't stand still, and the world
around it is not standing still - nor can we.

Thank you.

http://www.jlica.shuttlepod.org/Default.aspx?pageId=27417

Racism hits non-English speakers' health

2007-10-01T01:46:00.000-07:00

Published in Aids_Asia Mailing List, September 17, 2007

Racial discrimination is putting at risk the mental health of manyVictorians, a new government report has found.
The VicHealth report, More Than Tolerance: Embracing Diversity ForHealth, was based on a survey of more than 4,000 people.
It found almost two-in-five Victorians from non-English speakingbackgrounds reported they had been treated with disrespect, insultedor called names because of their ethnicity, with a small proportionof those saying they experienced discrimination often.
Of those who reported racial discrimination, 40 per cent said theysuffered discrimination at work, while 30 per cent were discriminatedagainst in an educational setting, the report said.Almost 45 per cent said they had a bad experience with racism at asporting or public event, while 19 per cent said they experiencedracism at the hands of police.
About one-third of Victorians said they could identify cultural orethnic groups they believed did not fit into Australian society.
The report revealed that those who suffered discrimination were morelikely to suffer poor mental health, smoke and misuse drugs oralcohol.
The findings tally with previous studies that showed an associationbetween discrimination and heart disease, diabetes and low infantbirth rate, VicHealth chief executive Todd Harper said.
People from migrant and refugee backgrounds continued tosuffer "unacceptably high levels of discrimination, in turn affectingtheir health and well-being", he said.
Former Australian Medical Association president Dr Mukesh Haikerwal,who is a GP in Melbourne's west, and who will help launch the report,said the report found a strong connection between racism and poormental health.
"The results of discrimination are a feeling of greater isolation andfeeling less connected with society," he said."That isolation and the very fact that they are racially abused means that they suffer ill-health including mental illness.
"We see this all the time in the west, of course, that people are newto the country, having trouble with the language and setting into anew life."They feel very upset and very much under the gun because of whattheir perceive as discrimination and poor support.
"Mr Harper said while the statistics on racism were striking, therewas also good news in the report."About 90 per cent of Victorian agreed that it was good to have asociety made up of different cultures, so I think that there is afair bit of support that we can build upon here," he said.
The report recommends a range of interventions, including furtherstudies, a range of communication and education campaigns andcommunity development programs to build networks between groups andcommunities.http://au.news.yahoo.com/070916/2/14ftb.html?=mv http://www.vichealth.vic.gov.au/discrimattitudes/

Asia's fishermen at risk for unwanted catch: HIV

2007-10-01T01:33:00.000-07:00

BALI, Indonesia (AP) — In appearance, they couldn't be more different.Ririn, with her warm brown skin and plump face, simply glows. Youngand sweet, just two months after giving birth to a baby girl.
Edi stands out as the roughest in a circle of men on the fishingdock. Streaks of motor oil mix with sweat on his chest and weather-beaten face as he puffs on a cigarette and talks loudly, not caringthat his frayed cutoffs are unzipped.
The two are part of an expanding nexus that's spreading HIV and AIDS.He's a deep-sea fishermen who spends his short time ashore prowlingfor sex; she's a woman in port who gets paid to provide a warm body.Bali is a famed tourist playground, but there's a side to the islandmost foreign visitors never see. Indonesian fishermen who oftenhaven't seen land for months put in at Benoa Harbour and makestraight for the closest bar with two things in mind: getting drunkand finding women.
These habits have put fishermen at high risk of getting HIV or AIDS -especially in Asia, because it's home to 2.5 million fishermen, orabout 85 per cent of the world's total. Yet fishermen have beenlargely overlooked since the virus began raging 21 years ago, withonly a handful of surveys focusing on them.
One report found that out of 10 poor countries, all but one hadfishermen with HIV rates four to 14 times higher than the generalpopulation.
Two studies of fishermen on big commercial vessels found over 15 percent were HIV-positive in Thai and Cambodian ports. That's more thanfive times the rate of other migrants at high risk for infection,such as truck drivers.A few programs in Papua New Guinea, Thailand and elsewhere in theregion are now working to reach fishermen, and the UN Food andAgriculture Organization earlier this year urged that they berecognized as high risk. But fishermen weren't even mentioned inUNAIDS' 630-page 2006 global report.
"I don't think there's been much targeting of treatment and healthservice availability," says Edward Allison, of The WorldFish Centerin Malaysia, who has researched HIV in fishermen.
The bulk of Asia's fishermen are small-scale operators who return tohome port frequently or stop at coastal fishing camps where women andbooze are readily available. Others work aboard bigger vessels formonths at a time.In Bali, most of the fishermen are bachelors in their 20s and 30sfrom Indonesia's main island of Java. Many come from conservativeMuslim farm families but have traded their traditions for a cultureof danger and machismo.
Some return to home port in Bali at voyage's end. Others fish wellbeyond native waters, docking as far away as South Africa, Sri Lanka,Spain and Panama. Either way, their pockets are filled with money andthe only women waiting ashore are those looking to get paid.
Ririn, who like many Indonesians uses only one name, grew up on arice farm with her parents and seven siblings on the island of Java.She dropped out of school in fifth grade.At 20, she was offered a chance for a better life, working as a maidon Bali, a neighbouring island she imagined was full of hope andmoney."I wanted to help my family back home," she says. "There's a lot ofmouths to feed."But after three months of cooking, cleaning and caring for someoneelse's children, she had only US$20.
Like many young women far from home, she was wooed by a man promising$40 to $50 a month for fewer hours. She would only do it for a littlewhile, she thought. Just long enough to save up for a small businessof her own.After six months as a prostitute, she learned about HIV - when shetested positive. She kept working until her sixth month of pregnancy.
There are no condom machines or AIDS outreach workers on the crowdedwharf in Bali. Some fishermen say they've had a disease "down there"or know someone who has, but many are convinced that certain women,mostly Indonesians, are free of HIV."This area is very safe," fisherman Herman Shokana said above theroar of boat engines. "But when we go abroad, we'll probably get it.
"Most sailors infected with STDs treat themselves with cheapantibiotics. They may take the wrong dose or stop treatment whensymptoms disappear, allowing STDs to linger, which makes it easier tocontract HIV. They also are misled by greedy peddlers.
"When the ships come in, medicine vendors or peddlers are alreadywaiting for them," said Made Setiawan, a doctoral student at theUniversity of Illinois, Chicago, who's researching fishing cultureand the risks of HIV in Bali. The peddlers' typical patterruns, "Here, take this medicine and go have sex in the brothels.
"In Thailand, most commercial fishermen are Cambodian and Burmesemigrants. They change boats regularly and go to different docks,making it difficult to visit clinics or get test results.At some Thai ports, outreach workers from the nonprofit Raks ThaiFoundation distribute condoms and talk to the men about AIDS. Somefishermen also are being trained to provide HIV education and helptreat STDs.
But experts say there's a need to establish STD clinics at ports andbetter educate the fishermen about everything from safe sex togetting infections at tattoo parlors."We're making progress," says Brahm Press, a program manager for RaksThai. "How much of that progress has been able to reduce the spreadof HIV, we're not certain.
"Edi, 20, is the shortest guy on the dock in Bali, but his muscles are the thickest. He's been on shore nearly two weeks after five straightmonths at sea fishing between Indonesia and Australia.
He brags he had sex with up to 10 women a night. His monthly pay ofabout $70 wouldn't have lasted long at the going rate of about $6 for15 minutes.
He usually doesn't use condoms, complaining it's not satisfying. He'snever been sick or tested for STDs, but points to a friend who's hadsyphilis."There's a medicine for HIV. There is a cure," he says. "Maybe itwill take longer to cure, but you will get better."While at sea, the men get little sleep and regularly risk injury or even death. They could be swept overboard in storms, get fouled inlines or cut off fingers while cleaning fish. They live in crampedboats smelling of diesel and gutted fish. Some question why theyshould lessen the little pleasure they get by wearing a condom.Some fishermen also insert BB-sized, glass or plastic pellets intocuts in their penises for enhancement. The wound is sometimes stillfresh when they make shore, but it doesn't stop them from hitting thebars lined with women in miniskirts."They don't have any self-esteem. They are ordered around by thecompany and the captain to do this and that," said Setiawan, who's researching the fishermen. "Sex workers can give them their self-esteem back.
"Ririn, 22, may sleep with up to 10 men a night. Many are fishermen.Worried she may infect a man who could then give HIV to his wife, shesometimes begs customers to wear condoms - which is more than anyonedid for her.
Most refuse.
"I tell them, 'I'm a working girl. There's a chance you might catchsomething from me,"' she says."The man says, 'That's tomorrow's problem.' "She fears, too, that her daughter Meisa may be infected, but it willtake 18 months for the test results.Now, Ririn's back on the street, still trying to earn enough to opena small shop. She hopes she can quit within a year, but realizes itwon't be easy. Especially with a hungry little one at home and asteady stream of fishermen like Edi, all in search of love for sale.
http://canadianpress.google.com/article/ALeqM5jhV4LiKEuDZPb_IOyuQ-FcoUmo_A

Editorial Review: The Role of Human Leukocyte Antigen E and G in HIV Infection

2007-07-12T16:22:00.000-07:00

http://www.medscape.com/viewarticle/559456

Introduction
An important area of HIV research is the immune response and how HIV circumvents it to create a successful and chronic infection. Various studies have provided not only a basic understanding of 'how HIV invades' but also clues for the development of vaccines to fight against AIDS. Although HIV initially evokes an immune response, it later escapes and evades the immune system for a successful infection. Methods of escape from the immune response include rapid mutations altering the organization of cell surface receptors, alterations in the expression profile of human leukocyte antigens (HLA) and destruction of immune effector cells.
HIV infects through exchange of body fluids. The cells mainly infected by HIV are the T helper cells (CD4 T cells), dendritic cells and macrophages. This tropism is generated because HIV utilizes CD4 as a primary receptor plus a coreceptor: CCR5 (expressed on macrophages, dendritic cells and T cells) for the R5 HIV strain and CXCR4 (T cells) for the X4 strain.[1] At the early stages of infection, HIVR5 utilizing CCR5 predominates, whereas at the later stages HIVX4 using CXCR4 is mainly seen.[2,3]

In the early stages of infection, the foremost target is CD4 T cells.[4] These cells along with other putative targets harbour mature virus and be carried in the circulation to lymph nodes and lymphoid organs. Here, the virions continue to infect immune cells, preferentially CD4 cells,[5] in some more vigorous way as the density of target cells are higher at these places. This infection as well as the destruction of CD4 cells later on leads to a profound decrease in CD4 cell count. The sudden depletion in CD4 T cells is unlikely to be caused simply by direct viral-induced lysis as the number of cells infected initially may not be sufficient to account for the massive decrease observed.[6] It has been suggested that bystander apoptosis induced by viral antigens or cytokines,[7,8] and downregulation of CD4 receptor by viral HIV-negative effector (Nef) protein,[9,10] may be involved. Other studies have emphasized apoptosis mediated by CD95 (FAS) and CD95L [FAS ligand (FasL)], which, in turn, are stimulated by increased concentration of viral envelope protein gp120 during infection, as a mechanism to account for the preferential depletion of CD4 T cells.[11,12]

With the continuing decrease in CD4 T cells, there is an explosive increase in virus production, which then evokes and is resisted by cellular immune response. After a peak of viral concentration has been reached, a gradual decrease is observed. Though activated cytotoxic T cells (CTL) can partially check infection,[13] which is evident by the appearance by HIV-specific CTL, this counterattack does not eradicate HIV completely as replicating viruses can escape the CTL response by mutation of their activation markers,[14] and through other mechanisms of immune escape. Some studies have suggested that this decline in virus concentration may be because of 'substrate exhaustion', as it is followed by depletion of CD4 T cells,[15,16] which functions as a reservoir for viral dissemination.

Cellular Immune Response to HIV Infection
HIV infection and intrusion of viral particles are counterattacked by CTL-mediated immune responses. Though the cellular immune response fails to control HIV-1 infection completely in most infected individuals, its occurrence is evident in regulating viral load during infection. During acute infection, reduction in viral load coincides with the appearance of HIV-specific CTL,[17,18] and an inverse relationship is established between viral load and HIV-specific CTL.[19] The initial CTL response may be directed against a few epitopes, which subsequently broadens during prolonged antigen stimulation.[20]

CTL could also be expected to have a role during chronic HIV-1 infection as HIV-1-specific T cells remain at high frequency.[21,22] The high concentration of these T cells may result from continued antigenic stimulation. This observation is supported by the fact that there is a steady decline in CTL as viraemia is reduced by HAART.[23] However, in chronic infection without treatment, a high number of HIV-1-specific CTL is seen. Though the CTL response occurs in early as well as in later stages of infection, the epitopes targeted during acute infection often differ from those recognized during chronic infection.[20,24]

When CTL recognize self-HLA molecules loaded with foreign peptide, they activate Fas and secrete perforins and granzymes, which lyse target cells.[25] The CTL produces cytokines (interferon α and tumour necrosis factor α) that affect viral replication.[26] HIV-1-specific CTL also produce the CC chemokines macrophage inflammatory protein 1α and 1β and RANTES, which suppress HIV-1 replication.[27] Even with these various effector functions, CTL cannot completely check viral intrusion in the immune system.

Immune Escape of Cytotoxic T Cells
As CTL do not carry CD4, the main receptor for viral entry and infection, they are anticipated to be a major player in HIV regulation. CTL can use multiple effector mechanisms to regulate viral replication,[25,28] including lytic mechanisms and CC chemokine-mediated blockade of viral entry.[29,30] The existence of HIV-specific CTL and their successful involvement in protection against disease transmission confirms their importance in disease regulation.[31,32]
As CTL can pose a strong regulatory force against HIV, virions that can escape the CTL response have a selection advantage. HIV has a high mutational rate (1 in 105 bases,[33]) and so can produce many mutants, but only those mutants that do not cost in terms of viral fitness would be selected. These mutational escapes lead to failure of vaccines as well as of immune regulation, as escape variants do not generate specific CTL but keep on eliciting the proliferation of CTL specific for wild type.[34] Escape mutations can work through many mechanisms, including alteration of epitopes presented on HLA for T cell receptors, lack of antigen processing, absence of improper interaction with HLA and finally lack of recognition by T cell receptors. During HIV infection, selective pressure imposed by CTL leads to the generation of various escape mutations and these variants may constitute the majority of the total viral pool. It has been shown that the ratio of non-synonymous substitutions to synonymous substitutions was higher in the CTL epitope. This further confirms the role of CTL selection pressure for occurrence and then for maintenance of these mutations.[35] Later on, evidence of escape mutations in HLA-B8-restricted epitope in Nef, HLA-B44-restricted epitope in Env and HLA-B27-restricted Gag epitope KK10 have supported the CTL-mediated selection of these mutations.[36]

Nef-Mediated Downregulation of Major Histocompatibility Complex Class I
In addition to escape mutations, HIV has strategies that can make the infected cell undetectable by the immune system. The detection of any cell depends on cell surface markers and so effective strategies alter the organization and expression of such markers. To escape from CTL response, HIV inhibits surface expression of the host major histocompatibility complex (MHC) class I, which is most important for CTL recognition; this is achieved through a viral protein called Nef. HIV-1 Nef is a 27-34 kDa multifunctional protein that has no apparent enzymatic activity but functions as an adaptor protein that enters the cell membrane through amino-terminal myristoylation. Though the exact mechanism by which Nef disrupts MHC class I cell surface expression is not clear, the viral protein binds to the cytoplasmic tail of the class I protein and may disrupt class I trafficking.[37] The cytoplasmic domain of class I antigens has a highly conserved region of 33 amino acid residues with nine conserved serine residues; Nef protein interacts with this via amino-terminal α-helix, polyproline and acidic domains.[38]
It was initially thought that Nef reduced MHC class I cell surface expression by accelerating endocytosis and promoting retrograde transport of internalized class I molecules to the trans-Golgi network (TGN).[39] Nef protein can interact with phosphofurin acidic cluster sorting protein 1 and then can activate phosphatidylinositol 3-kinase,[40] guanine exchange factor ARNO and finally ADP ribosylation factor 6.[41] This pathway leads to internalization of MHC class I molecules to 'ADP ribosylation factor compartments' that finally reach the TGN. However, more recent work has shown that Nef disrupts transport of MHC class I in the secretory pathway to the cell surface, rather than causing endocytosis from the cell surface. Further, it has been demonstrated that adaptor protein 1 (AP-1) is necessary for Nef to disrupt class I trafficking.[42] The main function of AP-1 is to sort proteins at the TGN by binding their cytoplasmic tails to clathrin and directing them to endolysosomal pathways.[43] Nef-mediated disruption of class I surface expression may occur by allowing interaction between the cytoplasmic tail of an MHC class I molecule and AP-1, thus redirecting the molecules from the TGN to the lysosomes for degradation,[42] as shown in Fig. 1. Recent work by Kasper et al.,[44] has shown that Nef targets MHC class I in T cells early in the biosynthetic pathway by preferentially binding newly synthesized hypophosphorylated class I molecules. The preferential interaction of Nef prevents phosphorylation of these molecules and so also prevents them reaching the cell surface In summary, the work of Collins and coworkers,[42,44] has demonstrated that Nef preferentially binds hypophosphorylated class I molecules, thus preventing completion of the secretory pathway that would finally provide an antigen-presenting receptor on the cell surface to activate killing of the virus-infected cell. Transport of class I molecules from the cell surface to the TGN occurs normally in infected cells but the class I molecules are then diverted to lysosomes through Nef-assisted binding of AP-1 to their cytoplasmic tail; this further inhibits their phosphorylation as well as their surface expression.

Figure 1.
Probable mechanism of viral HIV-negative effector (Nef)-mediated major histocompatibility complex class I internalization that may fail with human leukocyte antigen (HLA) G. Nef and adaptor protein (AP) 1 interact with the cytoplasmic domain of the class I in the trans-Golgi network (TGN) and then redirect class I protein-containing vesicles to the endolysosomal pathway. The truncated cytoplasmic domain of HLA-G makes Nef-mediated recycling ineffective as Nef proteins cannot dock on HLA-G and so surface expression of HLA-G does not change during HIV infection.

HLA Genotype and Cytotoxic T Cells
The HLA antigens activate cellular responses by forming the antigen-presenting component on the cell surface that interacts with CTL, directs them against the infected cells and activates natural killer (NK) cells of the innate immune response by interacting with the killer cell immunoglobulin-like receptor (KIR) family of surface molecules. There is substantial evidence that immune responses are effective in challenging the infection and transmission of HIV disease.
Though various genetic factors have been associated with susceptibility to HIV ( Table 1 ), investigations of the role of HLA antigens has concentrated on three areas: zygosity of HLA loci, sharing of alleles, and specific HLA allelic/haplotypic association with the outcome of disease. It has been shown that homozygosity at the class I loci is associated with relatively rapid progression to disease compared with heterozygotes.[54] This heterozygote advantage probably stems from the ability of such individuals to present a wider array of virus-derived epitopes to a more diverse CTL repertoire. This heterozygous repertoire will not only enable recognition and destruction of a greater breadth of infectious agents but will also require many more escape mutations for effective avoidance of the CTL response. Hence, heterozygosity may be associated with delayed progression to AIDS.[50] However, it is also conceivable that virus may become adapted and resistant to highly frequent alleles more easily in that population, and so a rare allele may have selective advantage in HIV disease progression.[55] The rare allele selective advantage may work in conjunction with heterozygote advantage, as the protective rare alleles are more likely to be present as heterozygotes.
Another genetic component that predisposes to the progression of AIDS is HLA sharing. Where the MHC class I is common to the donor and recipient, the basis of successful transplantation, it would lead to increased susceptibility to viral infection. One natural model of viral transmission between HLA-sharing donor and recipient is mother-to-child transmission, which further supports increased transmission of HIV in these circumstances.[56] Further, significant increase in susceptibility to HIV has been shown to be associated with concordance at the HLA-B locus but not at HLA-A or HLA-C.[57]
Knowing that a certain viral escape mechanism is likely to develop under a particular genetic selection pressure, it can be anticipated that an escape variant well adapted to a particular genetic profile and then transmitted to a host of similar genetic set up would be able to escape immunological challenges in the new host also. This may be a mechanism for susceptibility to viral transmission in hosts with HLA alleles in common. By comparison, MHC class I disparity may induce anti-HLA antibodies on passage of the virus and so may prevent HIV infection at early stages. Such a defence would be lacking in HLA concordant individuals, increasing successful transmission of HIV virus.
Previous research in genetic predisposition to viral susceptibility in the context of HLA has concentrated on specific alleles. Various studies have confirmed the contribution of specific class I alleles and more particularly HLA-B alleles in the outcome of disease.[58] This remarkable contribution of HLA-B may be because this group has the highest diversity among the class I antigens: approximately 661 alleles compared with 372 in HLA-A and 190 alleles in HLA-C.[59] Further, substantially greater selection pressure would be imposed on HIV by HLA-B compared with other class I antigens. Consistent association with delayed disease progression has been seen with HLA-B*27 and HLA-B*57.[51] Though the HIV HLA-B*57-specific epitope 'TW 10' may undergo an escape mutation, T242N, under selective pressure, this may cost in terms of viral fitness as the virus reverts after transmission to a new host.[60] Another allele, HLA-B*35, has been implicated as the class I susceptibility allele for AIDS.[52] HLA-B*35 heterozygotes have a rapid progression to AIDS, and homozygotes progress twice as fast as HLA-B*35-negative individuals. The most deleterious effects of HLA-B*35 are seen with its two subtypes, HLA-B*3502 and B*3503, which have proline at anchor position 2 of their loaded peptide and non-tyrosine residue at position 9.[52] By comparison, HLA-B*3501 containing tyrosine at position 9 does not have any substantial effect on disease prognosis. While both HLA-B*35 subtypes can equally induce a CTL response, viral load was cleared less effectively by non-tyrosine-containing HLA-B*3502 and B*3503 compared with HLA-B*3501.[61] It may, therefore, be possible that altered epitope recognition by HLA-B*3502 and B*3503 will induce CTL that may not specifically function against HIV-1-infected cells.
Some HLA-B alleles have been shown to influence the outcome of disease progression by interacting with KIR on NK cells. The Bw4 motif (residues 79-84 of the α3 domain) of various HLA-Bw4 alleles may interact with activating receptors KIR3DS1 of NK cells, thus facilitating clearance of HIV-1-infected lymphocytes and slowing disease progression.[62]
Studies have also been performed to examine particular MHC class II genes, but no consistent effects have been revealed. One recent study implicated the DRβ1*13-DQβ1*06 haplotype in viral suppression during treatment.[63]
Role of HLA-G and HLA-E in Progression of HIV Disease
Among the myriad of mechanisms adopted by HIV to avoid the human immune response is interference with the expression of HLA antigens. One evasion strategy is to downregulate cell surface class I classical antigens (HLA-A and HLA-B) to avoid HIV-specific CTL responses. Normally any change in the self HLA profile of cells is easily detected by immune surveillance and such cells are then subjected to degradation. However, despite reduced expression of class I antigens, HIV-infected cells are resistant to lysis by NK cells. During viraemic HIV-1 infection, there is expansion of an anergic subset of NK cells that do not respond to stimulation with MHC-devoid target cells. These NK cells have increased expression of SHIP (SH2-containing inositol phosphatase), which may be responsible for the reduced functional activity of these cells in chronic HIV-1 infection.[64] Various NK cell receptors that recognize MHC-independent ligands can regulate key cytolytic NK functions. A recent study has demonstrated that these inhibitory receptors recognizing an MHC-independent ligand are overexpressed in SHIP knockout mice and, therefore, may regulate NK cell cytolytic activity. This would suggest that SHIP plays an important role in regulation of this MHC-independent inhibitory NK receptor repertoire, which, in turn, is crucial for NK recognition and cytolysis of various targets.[65] However, this immunoprotection could also be achieved by increased expression of HLA-G and HLA-E during HIV infection. These antigens are less polymorphic than their classical counterparts. Where HIV Nef downregulates surface class I antigens by interacting with their cytoplasmic domain,[66] it may not be able to interact with non-classical HLA-I antigens such as HLA-G, which has a truncated domain,[67] (Fig. 1). Apart from any effects of the shorter cytoplasmic tail in HLA-G, it has been speculated that various mechanisms may upregulate HLA-G and HLA-E. The impact of these non-classical class I antigens on susceptibility to HIV infection is supported by their immunoregulating properties (Fig. 2).
Figure 2.
Upregulation of non-classical major histocompatibility complex class I human leukocyte antigen (HLA) antigens G and E by HIV as a strategy of immunodownregulation. HIV-negative effector (Nef) involved in class I downregulation does not affect HLA-G expression. HIV, through increased interleukin 10 (IL-10) during infection, can upregulate HLA-G expression, and viral peptide p24 amino acids 14-22 can upregulate HLA-E expression. Enhanced HLA-G and HLA-E can regulate natural killer (NK) cells by interacting with their inhibitory receptors. HLA-G can also control T cell response to HIV by directing T cells to apoptosis. KIR, killer cell immunoglobulin-like receptor; NKG2A, an NK-activating receptor.

HIV and HLA-G With a Truncated Cytoplasmic Domain
HLA G was cloned by Geraghty et al. in 1987.[67] It is less polymorphic, as only 15 alleles are known to date. It has restricted tissue distribution compared with the classical class I antigens. Though initially HLA-G was implicated in the maintenance of tolerance during pregnancy, its role has been explored in the tumour escape mechanism in various cancers and also in organ transplantation.
The exon organization of HLA-G is similar to the classical class I molecules, with three external domains (α1, α2, α3), a transmembrane domain and a cytoplasmic domain, and it is associated with β2-microglobulin to make the complete structure.[68] But HLA-G is more peculiar as it possesses a premature stop codon in exon 6 that results in a truncated cytoplasmic tail (it translates 6 amino acids instead of 30).[67] HLA-G exists in multiple isoforms, created by alternative splicing.[69] Seven different HLA-G transcriptional isoforms have been described; four of these encode membrane-bound forms whereas the remaining three encode soluble isoforms. HLA-G is identified as an immunoregulatory molecule as it can interact with inhibitory KIR of NK cells. So far, three HLA-G specific KIR have been identified: ILT-2 (LIR-1), ILT-4 (LIR-2) and KIR2DL4 ( Table 2 ).[74,75] In addition to acting via the innate mechanisms, HLA-G also provides protection through acquired immunity. HLA-G5 induces apoptosis of activated CD8 cells through activation of the Fas/FasL pathway,[76] whereas HLA-G1 suppresses CD4 lymphocyte proliferation.[77] Interaction of HLA-G1 with KIR of T cells can inhibit the antigen-specific HLA-restricted CTL response,[76] thus confirming the functionality of HLA-G in protecting cells from all possible immune responses.
HIV infection is characterized by loss of HLA-A and HLA-B, but the expression of HLA-G remains unaffected or at least not decreased. Along with inability of viral Nef to downregulate HLA-G, there could be some changes indirectly influencing the expression of HLA-G, particularly increased interleukin 10.[78] It has been shown that this cytokine upregulates expression of HLA-G.[79] Lozano et al.,[80] demonstrated the increased expression of HLA-G in all monocytes and some T lymphocytes after HIV infection. Other evidence had implicated HAART in upregulation of HLA-G,[81] but the study by Lozano et al.,[80] excluded this mechanism by showing elevated levels of HLA-G in untreated HIV-positive individuals. A contradictory report by Derrien et al.,[82] showed downregulation of HLA-G in HIV infection. Though these authors agreed that this was an Nef-independent process, as HLA-G is unable to interact with Nef, they thought it was more likely to be a viral protein U (Vpu)-dependent mechanism as HLA-G possesses a dilysine motif (RKKSSD) at -4 and -5 from the carboxy-terminus,[67] with which Vpu could interact and interfere with further intracellular trafficking of HLA-G. The difference between these two studies may arise for two reasons. First, Derrien et al.,[82] studied expression in cell lines, which would have subtle differences in microenvironment from in vivo. Second, the stage of infection may have a profound effect on the microenvironment, which, in turn, could alter HLA-G expression. Derrien et al.,[82] studied HLA-G expression in acute HIV infection, and their results are similar to other acute viral infections such as human cytomegalovirus and herpes simplex virus. These both decrease cell surface expression of HLA-G1, but the former particularly can increase HLA-G1 expression upon reactivation.[83,84] Possibly the expression of HLA-G could be enhanced in the natural course of HIV infection so that the situation in chronic infection would be as shown by Lozano et al..[80]
Further, HLA-G polymorphism is also associated with the risk of HIV infection. Matte et al.,[85] carried out an extensive study of HLA-G polymorphism in 456 HIV-seropositive and 406 HIV-seronegative African women and found significant association of G*0105N with protection from HIV-1 infection and G*010108 with susceptibility to infection. Allele G*0105N is characterized by deletion of cytosine at position 130 of exon 3, leading to frameshift and introduction of a stop codon in exon 4.[86] Hence allele G*0105N impedes production of a functional HLA-G molecule. The most likely reason for association of G*0105N with protection from HIV infection would be that this impairs the function of HLA-G and so downregulation by HIV would be absent or decreased. Recently Lajoie et al.,[53] presented more extended and explicit data for HLA-G polymorphism in the same cohort. They found that women carrying G*0105N had a 2.2-fold decreased risk of HIV-1 infection compared with women without G*0105N. They also reported an HIV- seronegative woman who was homozygous for G*0105N.
The G*010108 allele, reported to be associated with increased risk of HIV-1 infection,[85] has a synonymous substitution (proline) of G to A at codon 57. Though this mutation does not bring about any change in amino acid sequence, it is in the vicinity of Glu-63, which interacts with the P2 position of loaded peptide.[87] In the mouse homologue Qa-2, P1 arginine of the peptide interacts with Glu-62, Glu-63, Tyr-59 and Trp-167 residues, three out of four of which are in close proximity to Pro-57. Another HLA-G allele, G*010401, shares variation at codon 57 with G*010108, although it also has a non-synonymous substitution at codon 110. The G*010108/G*010401 genotype has been shown to have a greater association with increased risk of HIV infection.[85] However, this may be because G*010401 is a high secretor allele associated with increased secretion of soluble HLA-G molecules, consequently being open to more systemic downregulation. All individuals identified with G*010108/G*010401 were homozygous at codon 57.[85] Though this position is not directly involved in the presentation of peptide, zygosity of HLA at this position could still affect susceptibility to HIV infection. Aikhionbare et al.,[88] have shown that discordance at codon 57 of HLA-G exon 2 was significantly associated with non-transmission of HIV-1 infection in mother-child pairs studied to investigate the risk of perinatal HIV transmission. This is probably in agreement with the observations discussed above that HLA sharing leads to increased susceptibility to HIV-1 transmission. However, more studies are needed to validate these observations, particularly for HLA-G.
HIV and the Less Polymorphic HLA-E
HLA-E was initially recognized as HLA-6.2 and was mapped to chromosome 6p21.3 between HLA-C and HLA-A.[89] HLA-E has a wide tissue distribution including T cells, B cells, activated T lymphocytes and various other cells such as placenta cells and trophoblasts.[90,91] HLA-E is less polymorphic, having only three alleles identified so far. These three alleles can be differentiated as HLA-ER (0101) and HLA-EG (01031 and 01032) by a non-synonymous substitution of arginine by glycine at position 107. Alleles 01031 and 01032 differ only by a synonymous mutation at codon 77.
HLA-E also has NK-regulating properties, as HLA-E has been identified as a ligand of a subset of the immunoglobulin superfamily of NK cell receptors, and their interaction with KIR of NK cells may be responsible for inhibition of killer activities in these cells.[92] HLA-E is distinct in that it depends for surface expression on a highly conserved nonamer peptide derived from the signal sequence of other class I molecules including HLA-A, HLA-B, HLA-C and HLA-G, but not HLA-F.[93] The peptide structure is very important, as only appropriate peptide can be loaded onto HLA-E, enabling expression and subsequent protection of target cells by interaction of the HLA-E-peptide complex with the CD94/NKG2 receptor of NK cells.[94]
A potential role for HLA-E in susceptibility to HIV has been neglected until a recent report showed that it was upregulation during p24-positive HIV-1 infection.[95] Though HLA-E has wide tissue distribution, its dependency on peptides derived from MHC class I may affect its expression on HIV-1-infected cells, as they have decreased class I expression. However, HLA-E expression could be supported by peptides derived from HLA-G or of viral origin. There is evidence of HLA-E upregulation by viral peptides: UL40-derived peptide in human cytomegalovirus,[96] and core 35-45 peptide in herpes simplex virus.[97] It has also been shown that HLA-E is upregulated by peptide 14-22 derived from HIV p24. Comparison of the HIV p2414-22 peptide with the sequences of other known HLA-E-specific peptides showed that it was very similar, with only subtle changes, and matched the HLA-E-binding criteria. HIV p2414-22 shares isolucine at position 2, which appears to be essential for HLA-E interactions, and has residues at positions 4, 6 and 7 that are similar to those identified in other HLA-E-specific peptides. HIV p2414-22 peptide has asparagine at position 5, which may be essential for HLA-E-peptide complex interaction with CD94/NKG2A, an HLA-E-specific inhibitory NK cell receptor. It has been reported that upregulation of HLA-E by HIV p2414-22 can inhibit cytolytic function of NK cells by interacting particularly with inhibitory CD94/NKG2A receptor.
Specificity of this HLA-E-peptide complex interaction with CD94/NKG2A, responsible for inhibition of NK cell cytolysis, was further confirmed by studies that restored NK cell cytolytic activity by blocking HLA-E with specific monoclonal antibody 3D12 or blocking CD94/NKG2A with specific anti-NKG2A antibody.[98] The HLA-E-specific HIV p2414-22 peptide is derived from HIV Gag, and as it consists of a putative proteasome cleavage site, it is conceivable that the peptide could be processed by proteasomal cleavage during natural HIV infection.
There are reports relating to HLA-E polymorphism with susceptibility to HIV-1 infection. Lajoie et al.,[53] have demonstrated association of HLA-EG allele with protection against HIV infection. HLA-EG is known to have better immunoregulating properties than HLA-ER. HLA-EG has also been associated with other pathologies, for example nasopharyngeal carcinoma,[98] and affected pregnancy outcome.[99] Strong et al.,[94] have shown that HLA-EG-peptide complex always has higher surface expression than the HLA-ER-peptide complex and HLA-EG is also more thermally stable. When affinity with peptides of various origins was tested, it was found that the relative affinity of HLA-EG for peptide was significantly higher than that of HLA-ER.[94]
As there is substantial evidence for a role for HLA-EG in efficient immunoregulation, its association with better prognosis in HIV infection would be expected; yet the converse is observed, which further suggests that, under cellular stress, HLA-E upregulation instead of immunoprotection supports immunosurveillance. HLA-E can interact with the leader peptide derived from heat shock protein 60 (hsp60),[100] which is generated in response to cellular stress. However, presentation of hsp60-derived peptide on HLA-E would not be sufficient to inhibit NK cell cytolytic activity, as the HLA-E-peptide complex could not interact efficiently with CD94/NKG2A.[100] The same situation might also occur with the HIV-derived peptide. As KIR receptors specifically identify HLA-E complexed with cellular peptide in order to stimulate NK cell inhibition, complexes with non-cellular peptides might interfere with this recognition by the inhibitory receptor. Further HLA-EG has higher stability and affinity with peptide than HLA-ER [94] hence it may have a more rigid three-dimensional conformation - and even subtle changes could be identified by CD94/NKG2A. There is also the possibility that HLA-E could induce virus-specific CTL immune responses, as in the case of cytomegalovirus-derived peptide. However, these assumptions require extensive functional studies to validate the impact of HLA-E and HIV-derived peptide on NK cell receptors.
Table 1. Various Genetic Factors in HIV Susceptibility

Table 2. Interaction of Human Leukocyte Antigen G and E With Different Natural Killer Cell Receptors

References
1. Doms RW, Trono D. The plasma membrane as a combat zone in the HIV battlefield. Genes Dev 2000; 14:2677-2688.
2. Connor RI, Sheridan KE, Ceradini D, Choe S, Landau NR. Change in coreceptor use coreceptor use correlates with disease progression in HIV-1-infected individuals. J Exp Med 1997; 185:621-628.
3. Zhang Y, Lou B, Lal RB, Gettie A, Marx PA, Moore JP. Use of inhibitors to evaluate coreceptor usage by simian and simian/human immunodeficiency viruses and human immunodeficiency virus type 2 in primary cells. J Virol 2000; 74:6893-6910.
4. McDougal JS, Mawle A, Cort SP, Nicholson JK, Cross GD, Scheppler-Campbell JA, et al. Cellular tropism of the human retrovirus HTLV-III/LAV. I. Role of T cell activation and expression of the T4 antigen. J Immunol 1985; 135:3151-3162.
5. Douek DC, Brenchley JM, Betts MR, Ambrozak DR, Hill BJ, Okamoto Y, et al. HIV preferentially infects HIV-specific CD4+ T cells. Nature 2002; 417:95-98.
6. Brinchmann JE, Albert J, Vartdal F. Few infected CD4+ T cells but a high proportion of replication-competent provirus copies in asymptomatic human immunodeficiency virus type 1 infection. J Virol 1991; 65:2019-2023.
7. Finkel TH, Banda NK. Indirect mechanisms of HIV pathogenesis: how does HIV kill T cells? Curr Opin Immunol 1994; 6:605-615.
8. Ameisen JC, Capron A. Cell dysfunction and depletion in AIDS: the programmed cell death hypothesis. Immunol Today 1991; 12:102-105.
9. Greenberg M, DeTulleo L, Rapoport I, Skowronski J, Kirchhausen T. A dileucine motif in HIV-1 Nef is essential for sorting into clathrin-coated pits and for downregulation of CD4. Curr Biol 1998; 8:1239-1242.
10. Greenberg ME, Bronson S, Lock M, Neumann M, Pavlakis GN, Skowronski J. Co-localization of HIV-1 Nef with the AP-2 adaptor protein complex correlates with Nef-induced CD4 down-regulation. EMBO J 1997; 16:6964-6976.
11. Li Q, Duan L, Estes JD, Ma ZM, Rourke T, Wang Y, et al. Peak SIV replication in resting memory CD4+ T cells depletes gut lamina propria CD4+ T cells. Nature 2005; 434:1148-1152.
12. Boirivant M, Viora M, Giordani L, Luzzati AL, Pronio AM, Montesani C, Pugliese O. HIV-1 gp120 accelerates Fas-mediated activation-induced human lamina propria T cell apoptosis. J Clin Immunol 1998; 18:39-47.
13. Koup RA, Safrit JT, Cao Y, Andrews CA, McLeod G, Borkowsky W, et al. Temporal association of cellular immune responses with the initial control of viremia in primary human immunodeficiency virus type 1 syndrome. J Virol 1994; 68:4650-4655.
14. Borrow P, Lewicki H, Wei X, Horwitz MS, Peffer N, Meyers H, et al. Antiviral pressure exerted by HIV-1-specific cytotoxic T lymphocytes (CTLs) during primary infection demonstrated by rapid selection of CTL escape virus. Nat Med 1997; 3:205-211.
15. Phillips AN. Reduction of HIV concentration during acute infection: independence from a specific immune response. Science 1996; 271:497-499.
16. Schwartz EJ, Neumann AU, Teixeira AV, Bruggeman LA, Rappaport J, Perelson AS, et al. Effect of target cell availability on HIV-1 production in vitro. AIDS 2002; 16:341-345.
17. Borrow P, Lewicki H, Hahn BH, Shaw GM, Oldstone MB. Virus-specific CD8+ cytotoxic T-lymphocyte activity associated with control of viremia in primary human immunodeficiency virus type 1 infection. J Virol 1994; 68:6103-6110.
18. Koup RA, Safrit JT, Cao Y, Andrews CA, McLeod G, Borkowsky W, et al. Temporal association of cellular immune responses with the initial control of viremia in primary human immunodeficiency virus type 1 syndrome. J Virol 1994; 68:4650-4655.
19. Ogg GS, Jin X, Bonhoeffer S, Dunbar PR, Nowak MA, Monard S, et al. Quantitation of HIV-1-specific cytotoxic T lymphocytes and plasma load of viral RNA. Science 1998; 279:2103-2106.
20. Yu XG, Addo MM, Rosenberg ES, Rodriguez WR, Lee PK, Fitzpatrick CA, et al. Consistent patterns in the development and immunodominance of human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses following acute HIV-1 infection. J Virol 2002; 76:8690-8701.
21. Altman JD, Moss PA, Goulder PJ, Barouch DH, McHeyzer-Williams MG, Bell JI, et al. Phenotypic analysis of antigen-specific T lymphocytes. Science 1996; 274:94-96 [Erratum in Science 1998; 280:1821.].
22. Kuroda MJ, Schmitz JE, Charini WA, Nickerson CE, Lord CI, Forman MA, et al. Comparative analysis of cytotoxic T lymphocytes in lymph nodes and peripheral blood of simian immunodeficiency virus-infected rhesus monkeys. J Virol 1999; 73:1573-1579.
23. Ogg GS, Kostense S, Klein MR, Jurriaans S, Hamann D, McMichael AJ, et al. Longitudinal phenotypic analysis of human immunodeficiency virus type 1-specific cytotoxic T lymphocytes: correlation with disease progression. J Virol 1999; 73:9153-9160.
24. Goulder PJ, Altfeld MA, Rosenberg ES, Nguyen T, Tang Y, Eldridge RL, et al. Substantial differences in specificity of HIV-specific cytotoxic T cells in acute and chronic HIV infection. J Exp Med 2001; 193:181-194.
25. Berke G. The CTL's kiss of death. Cell 1995; 81:9-12.
26. Mosmann TR, Li L, Sad S. Functions of CD8 T-cell subsets secreting different cytokine patterns. Semin Immunol 1997; 9:87-92.
27. Wagner L, Yang OO, Garcia-Zepeda EA, Ge Y, Kalams SA, Walker BD, et al. Beta-chemokines are released from HIV-1-specific cytolytic T-cell granules complexed to proteoglycans. Nature 1998; 391:908-911.
28. Tschopp J, Hofmann K. Cytotoxic cells: more weapons for new targets? Trends Microbiol 1996; 4:91-94.
29. Cocchi F, DeVico AL, Garzino-Demo A, Cara A, Gallo RC, Lusso P. The V3 domain of the HIV-1 gp120 envelope glycoprotein is critical for chemokine-mediated blockade of infection. Nat Med 1996; 2:1244-1247.
30. Cocchi F, DeVico AL, Garzino-Demo A, Arya SK, Gallo RC, Lusso P. Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8+ T cells. Science 1995; 270:1811-1815.
31. Rowland-Jones SL, Nixon DF, Aldhous MC, Gotch F, Ariyoshi K, Hallam N, et al. HIV-specific cytotoxic T-cell activity in an HIV-exposed but uninfected infant. Lancet 1993; 341:860-861.
32. Looney DJ. Immune responses to human immunodeficiency virus type 1 in exposed but uninfected individuals: protection or chance? J Clin Invest 1994; 93:920.
33. Coffin JM. HIV population dynamics in vivo: implications for genetic variation, pathogenesis, and therapy. Science 1995; 267:483-489.
34. McAdam S, Klenerman P, Tussey L, Rowland-Jones S, Lalloo D, Phillips R, et al. Immunogenic HIV variant peptides that bind to HLA-B8 can fail to stimulate cytotoxic T lymphocyte responses. J Immunol 1995; 155:2729-2736.
35. Moore CB, John M, James IR, Christiansen FT, Witt CS, Mallal SA. Evidence of HIV-1 adaptation to HLA-restricted immune responses at a population level. Science 2002; 24; 296:1439-1443.
36. Goulder PJ, Phillips RE, Colbert RA, McAdam S, Ogg G, Nowak MA, et al. Late escape from an immunodominant cytotoxic T-lymphocyte response associated with progression to AIDS. Nat Med 1997; 3:212-217.
37. Williams M, Roeth JF, Kasper MR, Fleis RI, Przybycin CG, Collins KL. Direct binding of human immunodeficiency virus type 1 Nef to the major histocompatibility complex class I (MHC-I) cytoplasmic tail disrupts MHC-I trafficking. J Virol 2002; 76:12173-12184.
38. Mangasarian A, Piguet V, Wang JK, Chen YL, Trono D. Nef-induced D4 and major histocompatibility complex class I (MHC-I) down-regulation are governed by distinct determinants: N-terminal alpha helix and proline repeat of Nef selectively regulate MHC-I trafficking. J Virol 1999; 73:1964-1973.
39. Le Gall S, Erdtmann L, Benichou S, Berlioz-Torrent C, Liu L, Benarous R, et al. Nef interacts with the mu subunit of clathrin adaptor complexes and reveals a cryptic sorting signal in MHC I molecules. Immunity 1998; 8:483-495.
40. Swann SA, Williams M, Story CM, Bobbitt KR, Fleis R, Collins KL. HIV-1 Nef blocks transport of MHC class I molecules to the cell surface via a PI 3-kinase-dependent pathway. Virology 2001; 282:267-277.
41. Blagoveshchenskaya AD, Thomas L, Feliciangeli SF, Hung CH, Thomas G. HIV-1 Nef downregulates MHC-I by a PACS-1- and PI3K-regulated ARF6 endocytic pathway. Cell 2002; 111:853-866.
42. Roeth JF, Williams M, Kasper MR, Filzen TM, Collins KL. HIV-1 Nef disrupts MHC-I trafficking by recruiting AP-1 to the MHC-I cytoplasmic tail. J Cell Biol 2004; 167:903-913.
43. Robinson MS, Bonifacino JS. Adaptor-related proteins. Curr Opin Cell Biol 2001; 13:444-453.
44. Kasper MR, Roeth JF, Williams M, Filzen TM, Fleis RI, Collins KL. HIV-1 Nef disrupts antigen presentation early in the secretory pathway. J Biol Chem 2005; 280:12840-12848.
45. Samson M, Labbe O, Mollereau C, Vassart G, Parmentier M. Molecular cloning and functional expression of a new human CC-chemokine receptor gene. Biochemistry 1996; 35:3362-3367.
46. Bream JH, Young HA, Rice N, Martin MP, Smith MW, Carrington M, et al. CCR5 promoter alleles and specific DNA binding factors. Science 1999; 284:223.
47. Anzala AO, Ball TB, Rostron T, O'Brien SJ, Plummer FA, Rowland-Jones SL. CCR2-64I allele and genotype association with delayed AIDS progression in African women. University of Nairobi Collaboration for HIV Research. Lancet 1998; 351:1632-1633.
48. An P, Nelson GW, Wang L, Donfield S, Goedert JJ, Phair J, et al. Modulating influence on HIV/AIDS by interacting RANTES gene variants. Proc Natl Acad Sci USA 2002; 99:10002-10007.
49. Winkler C, Modi W, Smith MW, Nelson GW, Wu X, Carrington M, et al. Genetic restriction of AIDS pathogenesis by an SDF-1 chemokine gene variant. ALIVE Study, Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC). Science 1998; 279:389-393.
50. Tang J, Costello C, Keet IP, Rivers C, Leblanc S, Karita E, et al. HLA class I homozygosity accelerates disease progression in human immunodeficiency virus type 1 infection. AIDS Res Hum Retroviruses 1999; 15:317-324.
51. Kaslow RA, Carrington M, Apple R, Park L, Munoz A, Saah AJ, et al. Influence of combinations of human major histocompatibility complex genes on the course of HIV-1 infection. Nat Med 1996; 2:405-411.
52. Gao X, Nelson GW, Karacki P, Martin MP, Phair J, Kaslow R, et al. Effect of a single amino acid change in MHC class I molecules on the rate of progression to AIDS. N Engl J Med 2001; 344:1668-1675.
53. Lajoie J, Hargrove J, Zijenah LS, Humphrey JH, Ward BJ, Roger M. Genetic variants in nonclassical major histocompatibility complex class I human leukocyte antigen (HLA)-E and HLA-G molecules are associated with susceptibility to heterosexual acquisition of HIV-1. J Infect Dis 2006; 193:298-301.
54. Carrington M, Nelson GW, Martin MP, Kissner T, Vlahov D, Goedert JJ, et al. HLA and HIV-1:heterozygote advantage and B*35-Cw*04 disadvantage. Science 1999; 283:1748-1752.
55. Trachtenberg E, Korber B, Sollars C, Kepler TB, Hraber PT, Hayes E, et al. Advantage of rare HLA supertype in HIV disease progression. Nat Med 2003; 9:928-935.
56. Polycarpou A, Ntais C, Korber BT, Elrich HA, Winchester R, Krogstad P, et al. Association between maternal and infant class I and II HLA alleles and of their concordance with the risk of perinatal HIV type 1 transmission. AIDS Res Hum Retroviruses 2002; 18:741-746.
57. Dorak MT, Tang J, Penman-Aguilar A, Westfall AO, Zulu I, Lobashevsky ES, et al. Transmission of HIV-1 and HLA-B allele-sharing within serodiscordant heterosexual Zambian couples. Lancet 2004; 363:2137-2139.
58. Kiepiela P, Leslie AJ, Honeyborne I, Ramduth D, Thobakgale C, Chetty S, et al. Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA. Nature 2004; 432:769-775.
59. Marsh SG, Albert ED, Bodmer WF, Bontrop RE, Dupont B, Erlich HA, et al. Nomenclature for factors of the HLA system, 2004. Tissue Antigens 2005; 65:301-369.
60. Leslie AJ, Pfafferott KJ, Chetty P, Draenert R, Addo MM, Feeney M, et al. HIV evolution: CTL escape mutation and reversion after transmission. Nat Med 2004; 10:282-289.
61. Jin X, Gao X, Ramanathan M Jr, Deschenes GR, Nelson GW, O'Brien SJ, et al. Human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses for groups of HIV-1-infected individuals with different HLA-B*35 genotypes. J Virol 2002; 76:12603-12610.
62. Martin MP, Gao X, Lee JH, Nelson GW, Detels R, Goedert JJ, et al. Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. Nat Genet 2002; 31:429-434.
63. Malhotra U, Holte S, Dutta S, Berrey MM, Delpit E, Koelle DM, et al. Role for HLA class II molecules in HIV-1 suppression and cellular immunity following antiretroviral treatment. J Clin Invest 2001; 107:505-517.
64. Alter G, Suscovich TJ, Kleyman M, Teigen N, Streeck H, Zaman MT, et al. Low perforin and elevated SHIP-1 expression is associated with functional anergy of natural killer cells in chronic HIV-1 infection. AIDS 2006; 20:1549-1551.
65. Wahle JA, Paraiso KH, Costello AL, Goll EL, Sentman CL, Kerr WG. Cutting edge: dominance by an MHC-independent inhibitory receptor compromises NK killing of complex targets. J Immunol 2006; 176:7165-7169.
66. Schwartz EJ, Neumann AU, Teixeira AV, Bruggeman LA, Rappaport J, Perelson AS, et al. Effect of target cell availability on HIV-1 production in vitro. AIDS 2002; 16:341-345.
67. Geraghty DE, Koller BH, Orr HT. A human major histocompatibility complex class I gene that encodes a protein with a shortened cytoplasmic segment. Proc Natl Acad Sci USA 1987; 84:9145-9149.
68. Lala PK, Zdravkovic M, Aboagye-Mathiesen G, Guimond MJ. Functional roles of HLA-G in the human placenta: fact and fancies. In: Gupta SK, editor. Reproductive Immunology. New Delhi: Narosa; 1999. pp. 233-241.
69. Ishitani A, Geraghty DE. Alternative splicing of HLA-G transcripts yields proteins with primary structures resembling both class I and class II antigens. Proc Natl Acad Sci USA 1992; 89:3947-3951.
70. Navarro F, Llano M, Bellon T, Colonna M, Geraghty DE, Lopez-Botet M. The ILT2(LIR1) and CD94/NKG2A NK cell receptors respectively recognize HLA-G1 and HLA-E molecules co-expressed on target cells. Eur J Immunol 1999; 29:277-283.
71. Colonna M, Samaridis J, Cella M, Angman L, Allen RL, O'Callaghan CA, et al. Human myelomonocytic cells express an inhibitory receptor for classical and nonclassical MHC class I molecules. J Immunol 1998; 160:3096-3100.
72. Borrego F, Ulbrecht M, Weiss EH, Coligan JE, Brooks AG. Recognition of human histocompatibility leukocyte antigen (HLA)-E complexed with HLA class I signal sequence-derived peptides by CD94/NKG2 confers protection from natural killer cell-mediated lysis. J Exp Med 1998; 187:813-818.
73. Braud VM, Allan DS, O'Callaghan CA, Soderstrom K, D'Andrea A, Ogg GS, et al. HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C. Nature 1998; 391:795-799.
74. Rajagopalan S, Long EO. A human histocompatibility leukocyte antigen (HLA)-G-specific receptor expressed on all natural killer cells. J Exp Med 1999; 189:1093-1100.
75. Ponte M, Cantoni C, Biassoni R, Tradori-Cappai A, Bentivoglio G, Vitale C, et al. Inhibitory receptors sensing HLA-G1 molecules in pregnancy: decidua-associated natural killer cells express LIR-1 and CD94/NKG2A and acquire p49, an HLA-G1-specific receptor. Proc Natl Acad Sci USA 1999; 96:5674-5679.
76. Fournel S, Aguerre-Girr M, Huc X, Lenfant F, Alam A, Toubert A, et al. Cutting edge: soluble HLA-G1 triggers CD95/CD95 ligand-mediated apoptosis in activated CD8+ cells by interacting with CD8. J Immunol 2000; 164:6100-6104.
77. Bainbridge DR, Ellis SA, Sargent IL. HLA-G suppresses proliferation of CD4(+) T-lymphocytes. J Reprod Immunol 2000; 48:17-26.
78. Navikas V, Link J, Persson C, Olsson T, Hojeberg B, Ljungdahl A, et al. Increased mRNA expression of IL-6, IL-10, TNF-alpha, and perforin in blood mononuclear cells in human HIV infection. J Acquir Immune Defic Syndr Hum Retroviruses 1995; 9:484-489.
79. Moreau P, Adrian-Cabestre F, Menier C, Guiard V, Gourand L, Dausset J, et al. IL-10 selectively induces HLA-G expression in human trophoblasts and monocytes. Int Immunol 1999; 11:803-811.
80. Lozano JM, Gonzalez R, Kindelan JM, Rouas-Freiss N, Caballos R, Dausset J, et al. Monocytes and T lymphocytes in HIV-1-positive patients express HLA-G molecule. AIDS 2002; 16:347-351.
81. Cabello A, Rivero A, Garcia MJ, Lozano JM, Torre-Cisneros J, Gonzalez R, et al. HAART induces the expression of HLA-G on peripheral monocytes in HIV-1 infected individuals. Hum Immunol 2003; 64:1045-1049.
82. Derrien M, Pizzato N, Dolcini G, Menu E, Chaouat G, Lenfant F, et al. Human immunodeficiency virus 1 downregulates cell surface expression of the non-classical major histocompatibility class I molecule HLA-G1. J Gen Virol 2004; 85:1945-1954.
83. Fisher S, Genbacev O, Maidji E, Pereira L. Human cytomegalovirus infection of placental cytotrophoblasts in vitro and in utero: implications for transmission and pathogenesis. J Virol 2000; 74:6808-6820.
84. Onno M, Pangault C, Le Friec G, Guilloux V, Andre P, Fauchet R. Modulation of HLA-G antigens expression by human cytomegalovirus: specific induction in activated macrophages harboring human cytomegalovirus infection. J Immunol 2000; 164:6426-6434.
85. Matte C, Lajoie J, Lacaille J, Zijenah LS, Ward BJ, Roger M. Functionally active HLA-G polymorphisms are associated with the risk of heterosexual HIV-1 infection in African women. AIDS 2004; 18:427-431.
86. Ober C, Aldrich C, Rosinsky B, Robertson A, Walker MA, Willadsen S, et al. HLA-G1 protein expression is not essential for fetal survival. Placenta 1998; 19:127-132.
87. Clements CS, Kjer-Nielsen L, Kostenko L, Hoare HL, Dunstone MA, Moses E, et al. Crystal structure of HLA-G: a nonclassical MHC class I molecule expressed at the fetal-maternal interface. Proc Natl Acad Sci USA 2005; 102:3360-3365.
88. Aikhionbare FO, Hodge T, Kuhn L, Bulterys M, Abrams EJ, Bond VC. Mother-to-child discordance in HLA-G exon 2 is associated with a reduced risk of perinatal HIV-1 transmission. AIDS 2001; 15:2196-2198.
89. Koller BH, Geraghty DE, Shimizu Y, DeMars R, Orr HT. H.L.A.-E. A novel HLA class I gene expressed in resting T lymphocytes. J Immunol 1988; 141:897-904.
90. Boucraut J, Guillaudeux T, Alizadeh M, Boretto J, Chimini G, Malecaze F, et al. HLA-E is the only class I gene that escapes CpG methylation and is transcriptionally active in the trophoblast-derived human cell line JAR. Immunogenetics 1993; 38:117-130.
91. Houlihan JM, Biro PA, Harper HM, Jenkinson HJ, Holmes CH. The human amnion is a site of MHC class Ib expression: evidence for the expression of HLA-E and HLA-G. J Immunol 1995; 154:5665-5674.
92. Vales-Gomez M, Reyburn H, Strominger J. Molecular analyses of the interactions between human NK receptors and their HLA ligands. Hum Immunol 2000; 61:28-38.
93. Lee N, Goodlett DR, Ishitani A, Marquardt H, Geraghty DE. HLA-E surface expression depends on binding of TAP-dependent peptides derived from certain HLA class I signal sequences. J Immunol 1998; 160:4951-4960.
94. Strong RK, Holmes MA, Li P, Braun L, Lee N, Geraghty DE. HLA-E allelic variants. Correlating differential expression, peptide affinities, crystal structures, and thermal stabilities. J Biol Chem 2003; 278:5082-5090.
95. Nattermann J, Nischalke HD, Hofmeister V, Kupfer B, Ahlenstiel G, Feldmann G, et al. HIV-1 infection leads to increased HLA-E expression resulting in impaired function of natural killer cells. Antivir Ther 2005; 10:95-107.
96. Wang EC, McSharry B, Retiere C, Tomasec P, Williams S, Borysiewicz LK, et al. UL40-mediated NK evasion during productive infection with human cytomegalovirus. Proc Natl Acad Sci USA 2002; 99:7570-7575.
97. Nattermann J, Nischalke HD, Hofmeister V, Ahlenstiel G, Zimmermann H, Leifeld L, et al. The HLA-A2 restricted T cell epitope HCV core 35-44 stabilizes HLA-E expression and inhibits cytolysis mediated by natural killer cells. Am J Pathol 2005; 166:443-453.
98. Hirankarn N, Kimkong I, Mutirangura A. HLA-E polymorphism in patients with nasopharyngeal carcinoma. Tissue Antigens 2004; 64:588-592.
99. Tripathi P, Naik S, Agrawal S. HLA-E and immunobiology of pregnancy. Tissue Antigens 2006; 67:207-213.
100. Michaelsson J, Teixeira de Matos C, Achour A, Lanier LL, Karre K, Soderstrom K. A signal peptide derived from hsp60 binds HLA-E and interferes with D94/NKG2A recognition. J Exp Med 2002; 196:1403-1414.

Reprint Address
Professor Suraksha Agrawal, Department of Medical Genetics, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, Lucknow (UP) 226014, India. E-mail: suraksha@sgpgi.ac.in
Piyush Tripathi, Suraksha AgrawalFrom the Department of Medical Genetics, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, Lucknow (UP) 226014, India.

Increased prevalence of HIV: Not a casualty of war

2007-07-07T00:34:00.000-07:00

The Lancet 2007; 369:2187-2195, DOI:10.1016/S0140-6736(07)61015-0

Prevalence of HIV infection in conflict-affected and displaced people in seven sub-Saharan African countries: a systematic review

Dr Paul B Spiegel MD a , Anne Rygaard Bennedsen BSc b, Johanna Claass MD a, Laurie Bruns MA a, Njogu Patterson MD a, Dieudonne Yiweza MD a and Marian Schilperoord MA a

Summary

Background
Violence and rape are believed to fuel the HIV epidemic in countries affected by conflict. We compared HIV prevalence in populations directly affected by conflict with that in those not directly affected and in refugees versus the nearest surrounding host communities in sub-Saharan African countries.

Methods
Seven countries affected by conflict (Democratic Republic of Congo, southern Sudan, Rwanda, Uganda, Sierra Leone, Somalia, and Burundi) were chosen since HIV prevalence surveys within the past 5 years had been done and data, including original antenatal-care sentinel surveillance data, were available. We did a systematic and comprehensive literature search using Medline and Embase. Only articles and reports that contained original data for prevalence of HIV infection were included. All survey reports were independently evaluated by two epidemiologists to assess internationally accepted guidelines for HIV sentinel surveillance and population-based
surveys. Whenever possible, data from the nearest antenatal care and host country sentinel site of the neighbouring countries were presented. 95% CIs were provided when available.

Findings
Of the 295 articles that met our search criteria, 88 had original prevalence data and 65 had data from the seven selected countries. Data from these countries did not show an increase in prevalence of HIV infection during periods of conflict, irrespective of prevalence when conflict began. Prevalence in urban areas affected by conflict decreased in Burundi, Rwanda, and Uganda at similar rates to urban areas unaffected by conflict in their respective countries. Prevalence in conflict-affected rural areas remained low and fairly stable in these countries. Of the 12 sets of refugee camps, nine had a lower prevalence of HIV infection, two a similar prevalence, and one a higher prevalence than their respective host communities. Despite wide-scale rape in many countries, there are no data to show that rape increased prevalence of HIV infection at the population level.

Interpretation
We have shown that there is a need for mechanisms to provide time-sensitive information on the effect of conflict on incidence of HIV infection, since we found insufficient data to support the assertions that conflict, forced displacement, and wide-scale rape increase prevalence or that refugees spread HIV infection in host communities.

Affiliations

a. UN High Commissioner for Refugees, Geneva, Switzerland
b. University of Copenhagen, Copenhagen, Denmark

Correspondence to: Dr Paul B Spiegel, UN High Commissioner for Refugees, 94 rue de Montbrillant, 1202 Geneva, Switzerland. e-mail:
SPIEGEL@...

http://www.thelancet.com/journals/lancet/article/PIIS0140673607610150/fulltext

Half Of HIV Spread By Newly Infected

2007-07-03T04:25:00.000-07:00

Source:

McGill University

Date:

March 7, 2007

http://www.sciencedaily.com/releases/2007/03/070305084232.htm

Science Daily — A new study led by McGill University researchers shows that half of all HIV transmissions happen when newly infected people don’t know they are carrying the virus and may not even test positive for it.

The study, published in the April edition of the Journal of Infectious Diseases and already available online, followed 2,500 patients in eight Montreal HIV clinics over eight years. It showed that newly infected patients are eight times more likely to transmit the virus than those in the chronic stage of AIDS given the same behaviour.

Dr. Mark Wainberg, Director of the McGill AIDS Centre and internationally respected AIDS researcher, presented the findings at an academic AIDS conference in Los Angeles March 1 with lead author Dr. Bluma Brenner of the McGill Faculty of Medicine and the Jewish General Hospital.

“The most alarming thing is the confluence of a highly infectious state and the lack of awareness of that state,” said Dr. Wainberg. “It means we have to reconsider a lot of what we’re doing, both on the public education front and on the early intervention front.”

McGill Professor of Medicine and McGill University Health Centre (MUHC) AIDS researcher Dr. Jean-Pierre Routy, who was also instrumental in the study, said the Montreal urban population provided the ideal sample for the groundbreaking survey. “We had the infrastructure and the data here to get a comprehensive picture.” The study also involved researchers at Université de Montréal and at private and public AIDS clinics in the city.

The findings could change not only how soon people get tested after engaging in high-risk behaviour, but how they view that behaviour. “It has been shown that an HIV-positive diagnosis modifies high-risk behaviour,” said Dr. Wainberg. “So the more actively we can seek out and find newly infected people for testing and counselling, the better.”

Note: This story has been adapted from a news release issued by McGill University.

Are We Spending Too Much On HIV?

2007-07-03T04:21:00.000-07:00

Source:

BMJ-British Medical Journal

Date:

February 19, 2007

http://www.sciencedaily.com/releases/2007/02/070216113829.htm

Science Daily — Billions of pounds are being spent on the fight against AIDS in developing countries. In this week's British Medical Journal, two experts go head to head over whether we are spending too much.

HIV is receiving relatively too much money, with much of it used inefficiently and sometimes counterproductively, argues Roger England, Chairman of Health Systems Workshop.

Data show that 21% of health aid was allocated to HIV in 2004, up from 8% in 2000. It could now exceed a quarter. Yet HIV constitutes only 5% of the burden of disease in low and middle income countries as measured by disability adjusted life years lost (DALYs). It causes 2.8 million deaths a year worldwide -- fewer than the number of stillbirths, and much less than half the number of infant deaths. More deaths are attributable to diabetes than to HIV.

Furthermore, HIV interventions are not cost effective enough to justify this disproportionate spending, he writes. Much HIV money could be spent with more certain benefits on, for example, bed nets, immunisation, or family planning. Money is also wasted in areas that reflect the interests of those on the AIDS industry payroll more than evidence.

He believes that the money could be more effective if used to strengthen public health systems rather than focusing on disease-specific programmes.

AIDS is widely acknowledged as a public health crisis and current spending is woefully inadequate, argue Paul de Lay and colleagues at the Joint United Nations Programme on HIV and AIDS (UNAIDS).

Resources currently pledged are only half of what is needed for a comprehensive response. For instance, in 2006, $9bn was available for the AIDS response but the real need was estimated at $15bn. Poor coordination between different stakeholders in affected countries also impedes effective spending. This is compounded by weak institutions and regulatory policies, poor governance, and in some cases corruption.

They argue that the response to AIDS needs to be seen in the context of international commitments to the millennium development goals, which also call for progress across many other developmental priorities. HIV threatens many of these goals, especially those related to poverty and health.

The cost of inaction against AIDS is huge, far greater than for any other public health crisis, they say. Current costs are so high because of the inadequacy of previous investments, but they will be higher tomorrow if we continue to underinvest.

Note: This story has been adapted from a news release issued by BMJ-British Medical Journal.

DNA Vaccine Protects Against AIDS, Not HIV

2007-07-03T04:17:00.000-07:00

Source:	American Society For Microbiology
Date:	April 20, 2005

http://www.sciencedaily.com/releases/2005/04/050419105400.htm

Science Daily — While a new DNA vaccine may not be able to prevent HIV infection, it could protect against progression to full-blown AIDS. Researchers from Kansas report their findings in the March 2005 issue of the Journal of Virology.

Developing a vaccine to protect against HIV in attempt to gain control of the AIDS pandemic is a top priority for researchers throughout the world. Extensive testing has been conducted with live vaccines to determine if immunization would be effective at prevention, but they are not suitable for human use due to the potential that the vaccine viruses could mutate and reacquire the ability to cause disease.

DNA vaccines offer a new possibility for treatment. The have the advantages of safety, low cost of production, and ease of use in field conditions due to their minimal need for refrigeration.

In the study the DNA of a simian/human immunodeficiency virus (SHIV) was made noninfectious by removing the gene that makes reverse transciptase (a protein the virus requires to replicate). Four macaques were injected with the noninfectious vaccine, while two control animals remained unvaccinated. Both groups were challenged with SHIV. All four of the immunized macaques became infected with the challenge virus, but three survived. The two control subjects died.

"The results showed strong evidence that this type of vaccine could prevent AIDS and established that a DNA vaccine, such as this one, could be used alone, without the need for booster doses with viral proteins, for large-scale immunization programs," say the researchers.

(D.K. Singh, Z. Liu, D. Sheffer, G.A. Mackay, M. Smith, S. Dhillon, R. Hegde, F. Jia, I. Adany, O. Narayan. 2005. A noninfectious simian/human immunodeficiency virus DNA vaccine that protects macaques against AIDS. Journal of Virology, 79. 6: 3419-3428.)

Note: This story has been adapted from a news release issued by American Society For Microbiology.

Sri Lanka: Global AIDS Week of Action and response to G8

2007-06-17T17:09:00.000-07:00

Message 919, published in AIDS_ASIA mailing list on June 10, 2007

Commemorating the Global AIDS Week of Action

Sunday, June 3, 2007

Positive Hopes Alliance and Three Wheel Drivers' Collective against the spread of HIV and AIDS, two recently formed organizations supported by Action Aid to combat stigma and discrimination towards people living with HIV and AIDS in Sri Lanka, celebrated the candlelight ceremony to commemorate the Global Aids Week of Action on June 01 st 2007 at the welfare community centre at Anderson Flats, Colombo 05. Several activists participated at the vigil held at dusk.

In Sri Lanka, the candlelight ceremony was facilitated by Action Aid aims to raise awareness on the perspectives and priorities of people living with the virus well as to help maintain pressure on G8 countries to honour their 2005 pledge of universal treatment for all. The G8, the club of the eight richest countries will meet in Heiligendamm, Germany , next week (6-8 June).

"This is not just a ceremony where we want to raise awareness on HIV and AIDS and break stigma and discrimination in this country. It is also about campaigning for what governments promised two years ago, universal treatment for all," said Action Aid HIV/AIDS coordinator Rangapali Ranaweera

"In Sri Lanka we have started working with three wheel drivers as they can play a very important role on awareness raising and tackling stigma and discrimination. They are in contact with people from different backgrounds all the time and in that sense a well informed driver can be a fantastic tool to discuss informally about HIV related issues and promote some kind of social debate," said Action Aid HIV/AIDS coordinator Rangapali Ranaweera.

Governments worldwide are falling behind the internationally-accepted targets for AIDS treatment. "With more than 8,000 deaths and 15,000 new infections in the world everyday, there's definitely a need for action," affirmed Thilominie Chandrasekara from Positive Hopes. "In Sri Lanka the reported cases are only amounted to about 1,000 but the estimated figure is about 4,500. However, our country gathers some factors that can fuel the HIV epidemic such as the low level of awareness about HIV and AIDS or the risk behaviors which are on the rise."

There are only 1,000 reported cases in Sri Lanka, but the estimated figure is 4,500 according to the recent reports

HIV/AIDS activist demonstrates how to use a condom

http://2.bp.blogspot.com/_BL_iCCkYMKA/RmMwGGEc-7I/AAAAAAAABvo/Kyjcj349-40/s400/3+AIDS.jpg
Space Design street drama group performs a drama to create awareness on HIV/AIDS

http://3.bp.blogspot.com/_BL_iCCkYMKA/RmMpjWEc-4I/AAAAAAAABvQ/QJa5C8dJgc4/s400/4+AIDS.jpg
Kids enjoy the drama

AIDS quilt is being unfurled by activists

Sign for AIDS on the quilt

Candles are being lit by the participants

Candle light ceremony to commemorate the Global AIDS week of Action

Candles are lit to pay tribute to those who dies of AIDS all around the globe

A child lights a candle to pay tribute

Candle light vigil brought a climate of emotion in the venue

http://globalaidsweekofaction.blogspot.com/

By Dushiyanthini Kanagasabapathipillai ~ Contact Email: dushi.pillai@...

Malaysia: Negri makes pre-marital HIV test a must for Muslims

2007-06-17T17:05:00.000-07:00

SEREMBAN: From Friday, all Muslim couples getting married will have to undergo HIV tests in government clinics, Mentri Besar Datuk Seri Mohamad Hasan said.

"We want the couples to be free of any problem that can affect their family relationship," he said.

He said HIV and AIDS were among the top five diseases reported in the state, with 109 new cases reported last year but many cases went unreported because the victims had not gone for health checks. Mohamad said 80% of the 1,300 Muslim couples who attended pre-marital
courses last year were supportive of the tests to stem the spread of HIV/AIDS.

"This shows that prospective brides and grooms accept the idea and are conscious of their health," he said when contacted. Johor was the first to implement the ruling in 2001 before other
states followed suit.

"We will offer counselling and advice to those with HIV/AIDS to make them change their lifestyle," he said.

Mohamad said that in the Millennium Development Goals (MDG) report, it was stated that Malaysia had achieved all development targets except that of overcoming the HIV/AIDS issue.

"Malaysia is among the countries which are not free from HIV and AIDS due to the problems of drug misuse and the practice of free sex," he said.

Mohamad said statistics from the Health Ministry's AIDS and Sexually Transmitted Diseases division showed that 70,559 HIV cases were reported between 1986 and December 2005.

Some 10,663 patients had developed AIDS, of which 8,179 died.

http://thestar.com.my/news/story.asp?file=/2007/5/29/nation/17865980&sec=nation

Australia: PM wants to ban entry to people with HIV

2007-06-17T17:01:00.000-07:00

PM wants to ban entry to people with HIV

HIV-POSITIVE people should be banned from entering Australia, Prime Minister John Howard said yesterday, ignoring the advice of his health and immigration ministers who have told the PM that migrants carrying the disease are not a risk.

Mr Howard has said that leprosy sufferers should also be prevented from entering Australia.

"My view is the best result is that no one with those sort of ailments is allowed into the country," Mr Howard said on radio.

"I'm going to review the current position, and I want procedures put in place that see as far as possible that (HIV-positive people being allowed into Australia) doesn't happen. We are looking at it the next week or so."

But this week, a letter from Health Minister Tony Abbott and Immigration Minister Kevin Andrews advised the Prime Minister that people with HIV/AIDS should not be stopped from moving to Australia.

The Age believes the letter told the Prime Minister that HIV, unlike the airborne disease tuberculosis, is not highly contagious, and that blocking entry to HIV-positive people could be seen as discriminatory.

It is believed the departments have told the Prime Minister that immigration has not had a significant impact on HIV infection in Australia. In 2005, just 2 per cent of 928 new infections were contracted overseas, and half of that number were Australians or New Zealanders.

The Prime Minister's comments have been condemned by HIV/AIDS experts.

Executive director of the Australian Federation of AIDS Organisations, Don Baxter, said he was surprised by the Prime Minister's comments, especially as it conflicted with his Government's own advice.

"My only thought is that the PM must not have had time to look at the analysis from the departments which says a policy change is not necessary," Mr Baxter said.

He said the effect of refugees and migrants on the number of HIV infections was negligible.

"And it's already very difficult for people with HIV to migrate to Australia. All (HIV-positive) people are initially rejected, they then have to appeal, and very few are approved.

"Those that are are mainly partners, husbands or wives or same-sex partners of Australian citizens," Mr Baxter said.

"So I don't understand why the Prime Minister would want to introduce such punitive measures against Australian families. It seems illogical."

As well, an international HIV/ AIDS group has asked the Prime Minister to explain how HIV-positive visa-holders attending an international treatment and prevention conference in Sydney in July will be treated by his Government.

A letter from the European AIDS Treatment Group criticised Mr Howard for "fomenting stigma against people with HIV/ AIDS" and accused him of 19th century "isolationist measures".

"We find your plans, motivated, we suspect, purely by populism, disrespectful of our struggle against the disease that affects us."

http://www.theage.com.au/news/national/pm-wants-to-ban-entry-to-people-with-hiv/2007/06/01/1180205515105.html

Summary of what had transpired at G8 Summit 2007

2007-06-17T16:42:00.000-07:00

Published on AIDS_ASIA mailing list: message 923 June 13, 2007

G8 Summit 2007

G8 Pledges to Africa Insufficient, Some HIV/AIDS Advocates Say
G8 - Much Talk, Too Few Results
G8 Offers Vague Promises in the Face of Huge Epidemic
Commitments will be Honored
G8 Miss Mark as 'New' Announcements Disguise Overall Failure
G8 Leaders Pledge $60B To Fight HIV/AIDS, Fund Other Programs in Africa, Official Says
What news do I take home for my people?
Africa's brain drain here to stay
The J9 at the G8
Fear and stigma in rural South Africa
Fewer promises, more action
Canada at the 2007 G8 Summit
G8 leaders reach $60bn Aids deal
Aid agencies dismiss G8 aid pledge
Why women's silence kills
The value of protest
AIDS prevention paying the price of the G8 donor circus
G8 countries must invest more to achieve universal access targets – UNAIDS
G8 Considers Reducing Antiretroviral Drug Targets
G8 Appears To Be on 'Verge of Backtracking' on Gleneagles
G8 decision will spell death to millions with AIDS
G8 Summit Must Deliver on Two-Year Old Promises on Debt and HIV/AIDS
G8 - Africa on the Front Burner
Drug-Resistant AIDS - The Next Tsunami

****************************************

1. G8 Pledges to Africa Insufficient, Some HIV/AIDS Advocates Say

Kaisernetwork, 11 June 2007

Some HIV/AIDS advocates and other groups over the weekend criticized recent pledges from the Group of Eight industrialized nations to Africa as "insufficient" and "part of a pattern of unfulfilled promises," the Los Angeles Times reports (Retzlaff/Fleishman, Los Angeles Times, 6/9). G8 leaders in the final communique issued at the close of their summit in Heiligendamm, Germany, agreed to provide more than $60 billion to fight HIV/AIDS and address other issues in Africa.
http://www.kaisernetwork.org/daily_reports/rep_index.cfm?DR_ID=45475
---------------------------------

2. G8 - Much Talk, Too Few Results

Inter Press Service, 9 June 2007

This year's summit of the G8 heads of government will likely be remembered as a "how not to" organise such an event, for the contrast between the expectations it raised and its negligible
accomplishments, and for its enormous security costs.
http://allafrica.com/stories/200706090062.html
----------------------------------

3. G8 Offers Vague Promises in the Face of Huge Epidemic

Physicians for Human Rights, 8 June 2007

The Group of 8 has released the Africa section of the its 2007 communique, but AIDS advocates are dismayed by its vague language and lack of planning to meet ambitious goals, despite its promise to add $30 billion to US commitments.
http://allafrica.com/stories/200706080593.html
------------------------------------

4. Commitments Will be Honored

German Government, 8 June 2007

The discussions with African representatives were "very honest, very open" German Chancellor Angela Merkel said after the first working session on the last day of the Summit in Heiligendamm. US$60 billion have been pledged over the coming years to combat HIV/AIDS, malaria and tuberculosis.
http://allafrica.com/stories/200706080570.html
---------------------------------

5. G8 Miss Mark as 'New' Announcements Disguise Overall Failure

Oxfam International, 8 June 2007

G8 leaders are leaving Germany today having failed to do enough to shore up their wavering credibility or guarantee that they will keep their promises to Africa, said international agency Oxfam. Despite headline announcements of funds for HIV/AIDS and other diseases, the G8 has not got anywhere near back on track to meet overall promises on aid to Africa, and has missed the mark on areas like health and education.
http://allafrica.com/stories/200706080616.html
-------------------------------------

6. G8 Leaders Pledge $60B To Fight HIV/AIDS, Fund Other Programs in Africa, Official Says

Kaisernetwork.org, 8 June 2007

Leaders of the Group of Eight industrialized nations in the final communique issued at the close of their summit in Heiligendamm, Germany, agreed to provide more than $60 billion to fight HIV/AIDS and address other issues in Africa, Germany's Development Minister Heidemarie Wieczorek-Zeul announced Friday before G8 leaders met with African and international officials, the AP/International Herald Tribune reports (AP/International Herald Tribune, 6/8).
http://allafrica.com/stories/200706081041.html
-------------------------------------

7. What news do I take home for my people?

Africavox, 8 June 2007

As far as I can tell, everyone who's attended the G8 Summit here in Heiligendamm leaves it with mixed feelings. Some are bitter that the G8's announcement of $60 billion to fight disease failed to mention when it would arrive. Others complain that the Gleneagles promises have yet to be fulfilled.
http://panos.blogs.com/africavox2007/2007/06/what_news_do_i_.html
------------------------------

8. Africa's brain drain here to stay

Africavox, 8 June 2007

Underpaid, overworked and disillusioned: doctors and nurses are leaving Africa in droves. But the G8's response today offers nothing that will prevent further migration of Africa's healthcare workers.
http://panos.blogs.com/africavox2007/2007/06/africas_brain_d.html
----------------------------------

9. The J9 at the G8

Africavox, 8 June 2007

High school student Salwa Aman from Addis Ababa gives the impression of someone older than her years. And the 16-year-old has a lot on her mind. "There are a lot of street children in my country who are not able to learn. There are many children who lost their parents because of HIV/AIDS. It is hard to think about it," she says.
http://panos.blogs.com/africavox2007/2007/06/the_j9_at_the_g.html
-----------------------------------

10. Fear and stigma in rural South Africa

Africavox, 8 June 2007

The G8 has pledged extra funds for infectious diseases including HIV and AIDS. But a shortage of money is not the only barrier to HIV treatment. Fear, stigma and poverty are rife – and still claiming lives. Before coming to Germany, Zinhle Mapumulo visited one of many villages in South Africa where few are willing to discover their HIV status.
http://panos.blogs.com/africavox2007/2007/06/fear_and_stigma.html
--------------------------------

11. Fewer promises, more action

Africavox, 8 June 2007

Today's G8 'recommitment' to give $6-8 billion a year to fight HIV and AIDS, malaria and tuberculosis, has become the latest AIDS promise. And at this stage, it is still just that - a promise.
http://panos.blogs.com/africavox2007/2007/06/fewer_promises_.html
---------------------------------------

12. Canada at the 2007 G8 Summit

8 June 2007

At the conclusion today of his meetings with G8 and other leaders, Prime Minister Stephen Harper said that Canada had met its objectives for the Summit.
http://www.pm.gc.ca/eng/media.asp?id=1688
------------------------------------

13. G8 leaders reach $60bn Aids deal

BBC, 8 June 2007

G8 leaders meeting in Germany have vowed to deliver on pledges to Africa, and agreed a $60bn (£30bn) package for fighting Aids, malaria and TB.
http://news.bbc.co.uk/2/hi/europe/6732945.stm
-------------------------------------

14. Aid agencies dismiss G8 aid pledge

Guardian Unlimited, 8 June 2007

The leaders of the G8 today pledged to spend $60bn (£30bn) over the next few years on HIV/Aids, malaria and TB - a promise immediately dismissed by development groups as a smokescreen for the west's broken promises to the world's poor.
http://www.guardian.co.uk/g8/story/0,,2098552,00.html
----------------------

15. Why women's silence kills

Africavox, 7 June 2007

When she was ten years old her teacher raped her. At 14 her closest confidante, her church pastor, raped her. Now she is a mother, and she lives with HIV acquired during her marriage. The South African AIDS activist Nhkensani Mavasa rocked the G8 Alternative Summit with
her moving story.
http://panos.blogs.com/africavox2007/2007/06/why_womens_sile.html
-----------------------------------

16. The value of protest

Africavox, 7 June 2007

The last four days here in Germany have been dominated by the anti-globalisation protests. The roads are constantly blocked and the police keep telling us to take a different route.
http://panos.blogs.com/africavox2007/2007/06/the_value_of_pr.html
----------------------------------

17. AIDS prevention paying the price of the G8 donor circus

Africavox, 7 June 2007

G8 negotiators have spent much of the week in disagreement over a range of issues – including the commitment made two years ago at Gleneagles to increasing aid to Africa. As the Summit opened today, the prospects for Africa weren't looking bright.
http://panos.blogs.com/africavox2007/2007/06/aids_prevention.html
-----------------------------

18. G8 countries must invest more to achieve universal access targets - UNAIDS

PlusNews, 7 June 2007

Commitments on universal access to HIV prevention, treatment and care by leaders of the G8, the grouping of the world's richest countries, will not be met without additional resources, UNAIDS has warned.
http://www.plusnews.org/Report.aspx?ReportId=72610
-----------------------------------

19. G8 Considers Reducing Antiretroviral Drug Targets

UN Integrated Regional Information Networks, 7 June 2007

Leaders of the Group of Eight (G8), a grouping of some of the world's richest countries, are considering reducing their commitment to providing universal access to antiretroviral drugs, life-prolonging HIV/AIDS medication, by almost half, according to a statement released by the Zambian National AIDS Network (ZNAN).
http://allafrica.com/stories/200706070620.html
--------------------------

20. G8 Appears To Be on 'Verge of Backtracking' on Gleneagles HIV/AIDS Commitments, Financial Times Reports

Kaisernetwork.org, 7 June 2007

The Group of Eight industrialized nations appears to be on the "verge of backtracking" on commitments made at its 2005 summit in Gleneagles, Scotland, to provide universal access to HIV/AIDS treatment by 2010, the Financial Times reports. G8 leaders are meeting this week in Heiligendamm, Germany, for their annual summit (Williamson/Ward, Financial Times, 6/6).
http://allafrica.com/stories/200706071038.html
--------------------------------

21. G8 decision will spell death to millions with AIDS

World AIDS Campaign, 7 June 2007

As members of the Global Steering Committee for the World AIDS Campaign, we are shocked and alarmed that G8 leaders are reneging on their promise of universal access to treatment, care and prevention by 2010.
http://www.worldaidscampaign.info/index.php/en/media__1/press_releases/g8_decision_will_spell_death_to_millions_with_aids
-------------------------------

22. G8 Summit Must Deliver on Two-Year Old Promises on Debt and HIV/AIDS

Africa Action, 5 June 2007

The day before the Group of 8 (G8) wealthiest nations are to gather in Heiligendamm, Germany for their annual summit, Africa Action emphasized the lack of progress on key targets set by the G8 at their meeting in 2005 in Gleneagles, Scotland.
http://allafrica.com/stories/200706050906.html
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23. G8 - Africa on the Front Burner

This Day, 5 June 2007

This year's G8 Summit, taking place at Heiligendamm, Germany, is the 33rd edition of the annual meeting, which seeks to chart the way for industrialised nations to undergo subtle peer-review among themselves and also find ways to carry along developing countries in the quest for global integration in all aspects.
http://allafrica.com/stories/200706060092.html
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24. Drug-Resistant AIDS - The Next Tsunami

Accra Mail, 4 June 2007

At the forthcoming G8 summit in Germany, leaders are keen to play up their global citizenship by pledging millions more dollars to meet the UN's target of putting 10 million people on HIV/AIDS antiretroviral treatment by 2010.
http://allafrica.com/stories/200706041439.html

3GSM-Cell phones mobilised to fight AIDS in Africa

2007-06-17T16:36:00.000-07:00

Tue Feb 13, 2007 12:00am ET

BARCELONA, Feb 13 (Reuters) - Mobile phones are being harnessed to fight HIV/AIDS in Africa under a new $10-million scheme announced on Tuesday with the backing of leading companies and the U.S. government.

The "Phones-for-Health" project will use software loaded on to a standard Motorola (MOT.N: Quote, Profile , Research) handset to allow care workers in the field to enter critical health information into a central database in real time.

It will be transmitted using a standard GPRS mobile connection or, where this is not available, via an SMS channel.

The idea is to tap into the growing reach of mobile technology, which has leapfrogged older communication systems in many African countries.

Fixed-line telephone and Internet connections are rare across much of the continent, making pen and paper still the principal way of recording the spread of disease.

But more than 60 percent of Africans now live in areas with mobile phone coverage and that figure is expected to rise to 85 percent by 2010, according to the GSM Association, a global trade group representing leading mobile operators.

"The explosive spread of mobile phone networks across the developing world has created a unique opportunity to significantly transform how countries can tackle global health challenges," World Health Organization Assistant Director-General Howard Zucker said.

The new scheme builds on the success of a pilot project in Rwanda and will focus initially on the battle against HIV/AIDS in 10 African countries. South Africa's MTN (MTNJ.J: Quote, Profile , Research) is the first operator partner in the programme.

Longer term, the hope is that the scheme will be extended further in Africa and spread to Asia to address other infectious diseases, including malaria and tuberculosis, the partners behind the launch said at the 3GSM World Congress in Barcelona.

HIV And Malaria Fuel Each Other

2007-06-17T16:33:00.000-07:00

A study published in the Dec. 8, 2006 issue of Science supports the view that co-infection of HIV and malaria fuel each other. The study was conducted by the researchers from the Fred Hutchinson Cancer Research Center and the University of Washington at Kisumu, a town on the shores of Lake Victoria where there is a high incidence of malaria.

HIV is most easily spread when patients have high virus levels in their blood. Once a person with HIV contacts malaria, the level of the HIV virus surges by seven to ten times during a malaria fever episode. The surge may last up to eight weeks; but the patient recovers from the fever much earlier in intense malaria areas and becomes sexually active again. This significantly increases the risk of transmission of HIV to the sexual partner. On the other, persons with HIV are more susceptible to malaria, and so it continues.

This interaction between malaria and HIV infection may be causing both to spread more quickly in sub-Saharan Africa and this could explain why HIV is spreading more quickly than through sexual transmission alone in that region. The mathematical model applied in the study of an adult population of roughly 200,000 estimated that, since 1980, the disease interaction may have been responsible for 8,500 excess HIV infections and 980,000 excess malaria episodes. Co-infection might also have facilitated the geographic expansion of malaria in areas where HIV prevalence is high. The study concludes that transient and repeated increases in HIV viral load resulting from recurrent co-infection with malaria may be an important factor in promoting the spread of HIV in sub-Saharan Africa.

Source:
Laith J. Abu-Raddad, Padmaja Patnaik, James G. Kublin. Dual Infection with HIV and Malaria Fuels the Spread of Both Diseases in Sub-Saharan AfricaScience 8 December 2006: Vol. 314. no. 5805, pp. 1603 - 1606
Available at
http://www.sciencemag.org/cgi/content/abstract/314/5805/1603 http://www.sciencemag.org/cgi/data/314/5805/1603/DC1/1
http://mediconews.com/2006/12/09/hiv-and-malaria-help-each-other-spread/
http://timesofindia.indiatimes.com/NEWS/World/