The Body Covers: The 39th Annual Meeting of the Infectious Diseases Society of America
HIV/AIDS: Antiretroviral Therapy (Poster Session 87)
October 27, 2001
In one of those studies, 144 (40%) out of a total of 362 HIV-infected patients had GBV-C viremia in two tests. Forty-one of the patients with GBV-C viremia (28.5%) died during the follow-up period, as compared with 123 of the 218 patients who tested negative for GBV-C RNA (56.4%; p<0.001).
In addition, patients co-infected with the hepatitis G virus were found to have, on average, lower viral loads and higher CD4 counts than uninfected patients. Plus, they survive longer and have a decreased rate of CD4 loss. Before we discovered this fascinating bit of information, we never thought much about hepatitis G.
In any case, the one million dollar question remains: why? The answer, right now, is that we just do not know, and that is what makes this whole thing fascinating.
How can one viral infection prevent the progression of another infection? There are many theories. The most popular one now is that to some degree the immune response to hepatitis G "cross reacts" and also attacks HIV.
In this study, the Cleveland clinic group, with Michael Lederman and Hernan Valdez, looked at the response to antiretrovirals in patients infected with hepatitis G and compared it to the patients uninfected with hepatitis G, and surprise surprise, they found that patients with hepatitis G responded better! Maybe it is because they had a lower viral load to start with, but it did seem to be independent of that in the logistic regression analysis.
The results are very consistent in all the studies, and this does not seem to be a fluke. Hepatitis G (GBV-C) does something against HIV. We have not reached the point of intentionally infecting people with hepatitis G, but, hopefully, this study will help us to better characterize the immunologic response to HIV and eventually use this information for treatment and prevention. We will be hearing much more about this soon.
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