Background: GB virus C (GBV-C) viremia has recently been proposed to be associated with improved survival in HIV-infected subjects. We have assessed whether GBV-C status at diagnosis of HIV-1 infection can be used to predict the disease course in patients not receiving combination antiretroviral therapy, and whether longitudinal changes in GBV-C status occur during the course of HIV-1 infection.

Methods: We followed 230 HIV-1 infected patients (pts) until either death or initiation of combination therapy (median follow-up: 4.33 yrs). Markers for GBV-C infection (viremia:GBV-C RNA; resolved infection: anti-E2 antibodies [anti-E2]) were assessed in serum samples obtained within two years of HIV-1 diagnosis. From 163/230 patients, an additional sample obtained before the study endpoint was available for GBV-C testing. Kaplan-Meier survival curves were used for survival analysis.

Results: At baseline, GBV-C viremia was found in 62 pts (27%), and anti-E2 in 69 (30%). GBV-C viremia was less prevalent in pts presenting with AIDS (2/31) than in patients with asymptomatic infection (54/175; p = 0.008). No differences in mortality or AIDS incidence were observed with respect to baseline GBV-C status (p = 0.12 and 0.97, respectively). Similar results were obtained in 63 subjects with documented duration of HIV infection. During follow-up, 11/44 pts with GBV-C viremia at baseline lost GBV-C RNA without showing anti-E2 seroconversion. These pts were characterized by increased mortality (8/11 vs 16/89; p = 0.007), AIDS incidence (10/11 vs 19/70; p < 0.001), and a faster CD4⁺ cell decline (145 cells/mm³/year vs 56 cells/mm³/year; p = 0.006).

Conclusions: GBV-C status at diagnosis of HIV-1 infection does not predict the natural course of disease. The decreased prevalence of GBV-C viremia in patients with AIDS, and the observed loss of GBV-C viremia without anti-E2 seroconversion in patients with progressive disease support an interaction between these two viruses. However, the GBV-C status in HIV-1 infection is probably a secondary phenomenon during disease progression rather than an independent prognostic factor.