Do Hepatitis G/HIV coinfected patients do better on HAART? Debate revives

The debate concerning the clinical benefit for HIV-positive patients of coinfection with hepatitis G looks set to be revived. The 1^st February 2003 edition of the Journal of Infectious Diseases includes final data from a study conducted in the USA which shows that HIV/hepatitis G coinfected patients have a better response to HAART. These findings are in line with a study which found that hepatitis G was an independent predictor of HIV disease progression, but stand in stark contrast to studies presented to the Barcelona World AIDS Conference in 2002 which found no benefit from hepatitis G coinfection.

Investigators at the University Hospital of Cleveland, Ohio recruited all adult HIV-positive patients with a baseline CD4 count of below 200 cells/mm³ who started a protease inhibitor based HAART regimen between 1995 and 1997, to a study to establish if coinfection with hepatitis G improved response to HAART. Preliminary findings of this study were presented to the annual meeting of the Infectious Diseases Society of America in October 2001.

146 patients were included in the study, whose average CD4 count was 30 cells/mm³; viral load 160,000 copies/ml; and, age a little over 36 years. None of the patients had been treated with a protease inhibitor before, but over 36% had received either NRTI mono or dual therapy. The prevalence of hepatitis G RNA was 21.2% and antibodies associated with hepatitis G infection were found in 22.6% of patients.

Patients with hepatitis G RNA had significantly higher CD4 counts (60 cells/mm³ versus 30 cells) and lower HIV viral loads (125,000 copies/ml versus a little under 200,000 copies/ml) than patients with HIV alone.

When treated with HAART, patients coinfected with hepatitis G had a slightly larger increase in CD4 count (240 cells/mm versus 150 cells/mm³ and marginally larger fall in HIV viral load.

The investigators subjected their findings to multivariate analysis, and found that the only variables associated with a better response to HAART were hepatitis G coinfection and baseline HIV viral load.

Commenting on their findings the Ohio investigators observe that ”our results support the hypothesis”, that patients coinfected with hepatitis G “are more likely to respond to HAART than are patients with” HIV alone. The investigators acknowledge that coinfected patients had lower baseline HIV viral load and higher CD4 counts, however, “the magnitude of immunologic restoration by HAART, as reflected by an increase in CD4 cell count, was significantly larger in the coinfected group.” In addition, hepatitis G viremia “remained independently associated with virological treatment success after HAART.” This led the investigators to conclude that hepatitis G “coinfection itself exerts a beneficial effect on response to HAART that is not solely attributable to lower HIV RNA levels and higher CD4 counts observed in coinfected patients.”

However, studies presented to the International AIDS Conference in Barcelona in July 2002, found that there was no observable benefit from hepatitis G coinfection. Brumme’s study conducted amongst over 450 patients in Vancouver found that hepatitis G coinfection had no impact on “time to virological success…virological failure”, or “immunological failure”, concluding that hepatitis G coinfection “does not appear to have any effect on initial response to anti-HIV therapy.”

Moreover, a study conducted by Brust found that hepatitis G coinfection tended to worsen rather than improve survival.

The further investigations which the authors of the Ohio study call for in their conclusion should help establish if there really is any benefit (or otherwise) from hepatitis G coinfection.

Further information on this website

Infectious co-factors – hepatitis G