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The Body Covers: The 39th Annual Meeting of the Infectious Diseases Society of America

HIV/AIDS: Antiretroviral Therapy (Poster Session 87)

Coverage provided by Pablo Tebas, M.D.

October 27, 2001


Although we call it hepatitis G (GBV-C), this virus doesn't cause inflammation of the liver or any other illness that we know of. We usually say that it is a virus looking for a disease. However, the hepatitis G virus and its effect on HIV replication and progression has become one of the most interesting topics in HIV research since the back-to-back publication of two papers in the New England Journal of Medicine this September (see references, below).

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.


References

  1. Tillmann H. L., Heiken H., Knapik-Botor A. et al. Infection with GB Virus C and Reduced Mortality among HIV-Infected Patients. N Engl J Med 2001; 345:715-724, Sept. 6, 2001.

  2. Jinhua Xiang, Sabina Wunschmann, Daniel J. Diekemet al. Effect of Coinfection with GB Virus C on Survival among Patients with HIV Infection. N Engl J Med 2001; 345:707-714, Sept. 6, 2001.


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