No association between GB virus-C viremia and virological or immunological failure after starting initial antiretroviral therapy

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Abstract
Co-infection with GBV-C (`Hepatitis G’ virus) appears to be associated with slower disease progression in HIV-infected, untreated individuals. We wished to determine whether detection of GBV-C RNA was associated with differential response to HIV therapy in a population-based cohort of 461 individuals initiating antiretroviral therapy between June 1996 and August 1998, in British Columbia, Canada. The presence of GBV-C RNA in plasma was identified by nested RT–PCR, using detection of HIV gag RNA as a positive control. Time to virological success [achieving HIV plasma viral load (pVL) ≤ 500 copies/ml], virological failure (subsequent confirmed pVL > 500 copies/ml) and immunological failure (confirmed CD4 cell count below baseline) were assessed by Kaplan–Meier methods and Cox proportional hazard regression. Of the 441 individuals for whom results were available, 90 (20.4%) had detectable plasma GBV-C RNA. GBV-C RNA was significantly associated with a lower HIV pVL at baseline (P = 0.004). In univariate and multivariate Cox models, GBV-C RNA positive and negative individuals did not differ with respect to time to virological success [risk ratio (RR), 0.98; 95% confidence interval (CI), 0.75–1.27], time to virological failure (RR, 1.10; 95% CI, 0.74–1.65), or time to immunological failure (RR, 1.09; 95% CI, 0.73–1.63). There was no correlation between detection of GBV-C RNA and mutations in the human chemokine receptors CCR5 and CX3CR1, or HIV viral tropism as predicted by the HIV envelope sequence (P > 0.1). GBV-C viremia is relatively common in individuals seeking treatment for HIV infection; however, it does not appear to have any effect on initial antiretroviral therapy response.