Infection with harmless hepatitis G doesn't mean that HIV treatment works better

Infection with hepatitis G virus does not have any beneficial effects for patients taking antiretroviral therapy, a study has shown. Some earlier studies had suggested a survival benefit from infection with hepatitis G. However, in the November 1^st issue of the Journal of Acquired Immune Deficiency Syndromes investigators from a randomised trial into the safety and effectiveness of ritonavir-boosted protease inhibitors report that infection with hepatitis G virus did not mean that patients experienced a greater increase in their CD4 cell count after starting antiretroviral therapy; they were no more likely to achieve an undetectable viral load, and less likely to experience side-effects.

Several (but not all) studies have suggested that the course of HIV disease is less severe in individuals who are infected with hepatitis G virus (sometimes also called GB virus C or GBV-C). Although hepatitis G virus is related to hepatitis C virus, there is no evidence that it causes liver damage or illness in humans.

Some studies (but again, not all) have also indicated that anti-HIV therapy works more effectively in patients with hepatitis G infection.

The MaxCmin 1 trial was designed to compare the safety and efficacy of ritonavir-boosted saquinavir and indinavir. The study provided investigators with an opportunity to assess the impact of hepatitis G virus on the outcomes of antiretroviral therapy, within the context of a randomised controlled trial.

The investigators wished to see if after starting HIV treatment, infection with hepatitis G made any difference to CD4 cell gain; fall in viral load; rebound in viral load; and the occurrence of moderate to severe side-effects.

A total of 34% of patients were infected with hepatitis G at baseline. There were no significant demographic differences between hepatitis G-positive and hepatitis G-negative patients. The investigators also established that there were no statistical differences in CD4 cell count at baseline between patients who were infected with hepatitis G (median 260 cells/mm³) and negative for hepatitis G (median 280 cells/mm³). Nor did the lowest ever CD4 cell count differ between hepatitis G-positive (109 cells/mm³) and negative patients (120 cells/mm³).

After 48 weeks of anti-HIV therapy, the median increase in CD4 cell count was similar between hepatitis G-infected and uninfected individuals (median 74 cells/mm³). Amongst patients who experienced an increase in their CD4 cell count of 100 cells/mm³ or more after starting antiretroviral therapy, there was no statistically significant difference in the time to this outcome between hepatitis G-positive (median 12 weeks) and hepatitis G-negative (median 14 weeks) patients.

Although baseline viral load was marginally higher amongst patients infected with hepatitis G, similar proportions of infected and uninfected patients achieved an undetectable viral load. A total of 55 patients experienced a rebound in their viral load, and once again, infection with hepatitis G was not a significant factor.

Finally, the investigators noted that a similar proportion of hepatitis G-positive (32%) and hepatitis G-negative (35%) patients experienced moderate or severe side-effects.

“In this study we could neither observe any influence of GBV-C on any of the prognostic markers of HIV-1 infection at baseline nor on the response to HAART in prospective data”, write the investigators.

They add, “we…cannot exclude that GBV-C might be beneficial during the early period of HIV infection but might not be beneficial once the disease has progressed.” They also wonder if the possible positive effects of hepatitis G “might be blunted by the very strong effect of HAART itself.”