Hepatitis G virus infection in hepatitis C virus‐positive patients co‐infected or not with hepatitis B virus and/or human immunodeficiency virus

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Abstract
This was a retrospective study to evaluate the prevalence and impact of hepatitis G virus (HGV) infection in hepatitis C virus (HCV)‐positive drug addicts, according to the serological status of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) co‐infection. Two hundred and thirty‐five randomly selected intravenous drug addicted patients (147 French, 88 Italian) were studied. All patients were positive for antibodies to HCV (anti‐HCV). HGV RNA positivity was measured by reverse transcriptase–polymerase chain reaction (RT–PCR). Comparisons of HCV RNA positivity rate, and biological and histopathological variables, were made between HGV RNA‐positive and negative patients, according to their HBV and HIV status. HGV prevalence was around 30% in both French and Italian groups. No clear association between HGV infection and a particular HCV genotype was observed. The rate of HCV RNA positivity did not differ between HGV‐positive and HGV‐negative patients after stratification for hepatitis B surface antigen (HBsAg) and HIV positivity. Histological severity of the underlying chronic hepatitis did not differ according to the HGV status; however, in HIV‐positive HBsAg‐negative patients, the hepatitis activity was moderately increased in HGV‐positive patients. A striking negative influence of HBsAg positivity on HCV replication was observed in HIV‐negative patients: an HCV RNA‐positive rate of 25% was found in HBsAg‐positive patients vs 86% in HBsAg‐negative patients; similar significant results were observed in HIV‐positive patients, although to a lesser extent. The underlying chronic hepatitis was significantly more severe in HBsAg‐positive than in HBsAg‐negative HIV‐negative patients. Hence, HGV infection is highly prevalent in anti‐HCV positive drug addicts but the co‐infection with HCV does not seem to influence HCV replication nor to worsen the underlying chronic hepatitis, in HIV‐negative patients at least. Reciprocal influence between HBV, HCV and HIV appears rather complex, HBsAg carriage seeming to exert per se a negative effect on HCV replication, particularly in HIV‐negative patients, suggesting that interactions between hepatitis viruses should always be analysed in the light of HIV status.

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