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Treatment and the other virus—HIV-2

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Worldwide, most cases of AIDS are caused by infection with HIV-1. However, in parts of West Africa, a second type of immunodeficiency virus, called HIV-2, is more common. As people travel to and emigrate from this region, HIV-2 has gradually spread to other countries and regions, including Western Europe, India and North America. The first case of HIV-2 infection in Canada was detected in 1988.

Infection with HIV-2 initially has a different impact than HIV-1. For instance, the immune systems of people with HIV-2 generally degrade more slowly than those of people who are positive for HIV-1. Ultimately, the effects of HIV-2 infection are the same as HIV-1: AIDS.

Therapy in the lab
Most approved anti-HIV drugs have been designed to attack HIV-1. Until recently, their effect on HIV-2 was not well studied. Researchers in Leuven, Belgium, conducted lab tests to get an idea of the activity of these drugs against HIV-2. They found that HIV-2 was generally sensitive to nucleoside analogues (nukes), such as AZT (Retrovir, zidovudine), and nucleotide analogues, such as tenofovir (Viread). However, HIV-2 was able to resist the effects of non-nukes efavirenz (Sustiva, Stocrin) and nevirapine (Viramune) and the fusion inhibitor T-20 (Fuzeon, enfuvirtide). Most protease inhibitors appeared to have some degree of activity against HIV-2.

More recently, Spanish researchers, focusing on protease inhibitors (PIs), found that the following PIs have activity against HIV-2:

indinavir (Crixivan)
lopinavir (in Kaletra)
saquinavir (Invirase)
tipranavir (Aptivus)

Therapy in people
To begin to explore the effect of treatment in people with HIV/AIDS (PHAs) who were HIV-2 positive, researchers in Paris, France, performed a clinical trial for two years. They found a slow and small increase in CD4+ cell counts despite a significant decrease in viral load. For the study team, these results raise questions about which regimens should be used for HIV-2. As treatment programs are increasingly established in West Africa, this issue will become more pressing.

Study details
For several years, doctors in Paris have been monitoring the health of 458 PHAs who are HIV-2 positive. Doctors gave 61 participants combination therapy with regimens based on one of the following:

a combination of three nukes
two nukes and a protease inhibitor
two nukes and two protease inhibitors

Before starting therapy, participants’ average CD4+ count was 136 cells and their average viral load was 1,300 copies. Bear in mind that in HIV-2 infection viral loads are sometimes lower than average when compared to HIV-1 infection.

Results
After one year, the CD4+ count increased by an average of 41 cells. At no time during the first year was the increase in CD4+ cells ever significantly different from pre-study levels. During the second year, increases were also not significantly different from pre-study levels.

Researchers also checked the concentration of anti-HIV medications in the blood of 42 participants. Most participants had adequate levels of anti-HIV drugs, but eight did not, suggesting difficulties with absorption or inadequate adherence. Yet, over the long term, CD4+ cell counts did not significantly differ between these two sub-groups of PHAs.

Suppression of HIV replication did not differ by the type of treatment regimen. Over the course of the study, only 55% of participants had HIV that was below the 100-copy mark (the lower limit of the viral load assay used in this study).

Researchers are not sure why they observed such disappointing immunologic results, but they hope that other doctors in Western Europe can confirm or refute their findings.

Researchers in Boston and New York City have also documented the poor immunologic response to these medications in PHAs who have HIV-2. These researchers have called for clinical trials in HIV-2 positive people so that appropriate treatment guidelines can be devised.

—Sean R. Hosein

REFERENCES:

1. Nuvor SV, van der Sande M, Rowland-Jones S, et al. Natural killer cell function is well preserved in asymptomatic human immunodeficiency virus (HIV-2) infection but similar to that of HIV-1 infection when CD4 cell counts fall. Journal of Virology 2006;80(5):2529-2538.

2. Neumann PW, Lepine D, Woodside M, et al. HIV-2 infection detected in Canada. Canadian Diseases Weekly Report 1988;14(28):125-6.

3. Ren J, Bird LE, Chamberlain PP, et al. Structure of HIV-2 reverse transcriptase at 2.35-A resolution and the mechanism of resistance to non-nucleoside inhibitors. Proceedings of the National Academy of Sciences USA 2002;99(22):14410-14415.

4. Witvrouw M, Pannecouque C, Switzer WM, et al. Susceptibility of HIV-2, SIV and SHIV to various anti-HIV-1 compounds: implications for treatment and postexposure prophylaxis. Antiviral Therapy 2004;9:57-65.

5. Rhodes B, Sheldon J, Toro C, et al. Susceptibility to protease inhibitors in HIV-2 primary isolates from patients failing antiretroviral therapy. Journal of Antimicrobial Chemotherapy 2006; in press.

6. Matheron S, Damond F, Benard A, et al. CD4 cell recovery in treated HIV-2-infected adults is lower than expected: results from the French ANRS CO5 HIV-2 cohort. AIDS 2006;20(3):459-461.

7. Mullins C, Eisen G, Popper S, et al. Highly active antiretroviral therapy and viral response in HIV type 2 infection. Clinical Infectious Diseases 2004;38:1771-1779.

Created on: 03/01/2006

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