ObjectivesTo conduct a meta-analysis to synthesize the evidence regarding the effect of co-infection with GB virus C (GBV-C) on survival of HIV-infected individuals, and to estimate the effect. MethodsA Bayesian meta-analysis was conducted to synthesize evidence from eligible studies. Prospective survival studies of HIV-1-infected individuals, with outcome defined as time from baseline to allcause death, were included and classified by whether GBV-C status was determined in early or late HIV disease. The primary measure was the hazard ratio (HR) of death for HIV-infected individuals with GBV-C infection versus those without GBV-C infection. ResultsEleven studies from eight publications met the inclusion criteria. For studies with GBV-C status measured 2 years or less after HIV seroconversion (912 subjects), the combined HR was 0.88 [95% credible interval (CI) 0.30, 1.50]. For studies with GBV-C status measured more than 2 years after HIV seroconversion (1294 subjects), the combined HR was 0.41 (95% CI 0.23, 0.69). ConclusionsNo conclusive evidence was found of an association between survival and GBV-C infection early in HIV disease. However, when GBV-C infection was present later in HIV disease, a significant reduction in the hazard for mortality was observed for those with co-infection. Potential explanations for this difference include a non-proportional benefit of GBV-C over time, possibly related to clearance of GBV-C infection early in HIV disease. The timing of GBV-C infection appears to account for the contradictory results of studies on the effect of GBV-C coinfection on survival of HIV-infected people.Keywords: Bayesian meta-analysis, GB virus C, hepatitis G virus, HIV, survival Introduction GB virus C (GBV-C) and hepatitis G virus are RNA viruses that were independently identified in 1995, and were subsequently found to be two isolates of the same virus [1,2]. Although GBV-C was initially thought to be associated with chronic hepatitis, extensive investigation failed to identify any association between this virus and any clinical illness [3][4][5][6][7]. GBV-C is, phylogenetically, closely related to hepatitis C virus, but appears to replicate primarily in lymphocytes, and poorly if at all in hepatocytes [4][5][6][7][8].The majority of immune-competent individuals appear to clear GBV-C viraemia within the first few years following infection [7,9] and although the time interval between GBV-C infection and clearance of viraemia (detection of GBV-C RNA in plasma) is not known, infection may persist for decades in some individuals. Approximately 2% of healthy US blood donors are Conflict of interest: JTS has a patent on an infectious GBV-C clone. Parenteral, sexual and vertical transmission of GBV-C have all been documented, and because of shared modes of transmission, individuals infected with HIV are commonly co-infected with GBV-C. Among people with HIV infection, the prevalence of GBV-C viraemia ranges from 14 to 43% [4,5]. Since 1998, several studies have examined the effect of GBV-C infection at base...
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