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

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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 1st 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.

Glossary

boosting agent

Booster drugs are used to ‘boost’ the effects of protease inhibitors and some other antiretrovirals. Adding a small dose of a booster drug to an antiretroviral makes the liver break down the primary drug more slowly, which means that it stays in the body for longer times or at higher levels. Without the boosting agent, the prescribed dose of the primary drug would be ineffective.

statistical significance

Statistical tests are used to judge whether the results of a study could be due to chance and would not be confirmed if the study was repeated. If result is probably not due to chance, the results are ‘statistically significant’. 

efficacy

How well something works (in a research study). See also ‘effectiveness’.

prospective study

A type of longitudinal study in which people join the study and information is then collected on them for several weeks, months or years. 

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.”

References

Tillman HL et al. Impact of coinfection with HIV-1 and GB virus C in patients receiving a ritonavir-boosted HAART regimen: a substudy of the MaxCmin 1 trial. J Acquir Immune Defic Syndr 40: 378 – 380, 2005.