Infection with GB virus C and reduced mortality among HIV-infected patients.

Background: The flavivirus GB virus C (GBV-C, also designated hepatitis G v irus) was identified in a search for hepatitis viruses, but no disease is c urrently known to be associated with it. We investigated the relation betwe en coinfection with GBV-C and the long-term outcome in patients infected wi th the human immunodeficiency virus (HIV). Methods: A total of 197 HIV-positive patients were followed prospectively b eginning in 1993 or 1994. Of these patients, 33 (16.8 percent) tested posit ive for GBV-C RNA, 112 (56.9 percent) had detectable antibodies against the GBV-C envelope protein E2, and 52 (26.4 percent) had no marker of GBV-C in fection and were considered unexposed. We assessed the relation between GBV -C infection and the progression of HIV disease. We also tested 169 GBV-C-p ositive plasma samples with a quantitative branched-chain DNA (bDNA) assay in order to investigate possible correlations between GBV-C viral load and both the CD4+ cell count and the HIV load. Results: Among the patients who tested positive for GBV-C RNA, survival was significantly longer, and there was a slower progression to the acquired i mmunodeficiency syndrome (AIDS) (P<0.001 for both comparisons). Survival af ter the development of AIDS was also better among the GBV-C-positive patien ts. The association of GBV-C viremia with reduced mortality remained signif icant in analyses stratified according to age and CD4+ cell count. In an an alysis restricted to the years after highly active antiretroviral therapy b ecame available, the presence of GBV-C RNA remained predictive of longer su rvival (P=0.02). The HIV load was lower in the GBV-C-positive patients than in the GBV-C-negative patients. The GBV-C load correlated inversely with t he HIV load (r=-0.33, P<0.001) but did not correlate with the CD4+ cell cou nt. Conclusions: Coinfection with GBV-C is associated with a reduced mortality rate in HIV-infected patients. GBV-C is not known to cause any disease, but it is possible that its presence leads to an inhibition of HIV replication . However, GBV-C infection could also be a marker for the presence of other factors that lead to a favorable HIV response.