HEPATITIS-G VIRUS-INFECTION IN HEPATITIS-C VIRUS-POSITIVE PATIENTS CO-INFECTED OR NOT WITH HEPATITIS-B VIRUS AND OR HUMAN-IMMUNODEFICIENCY-VIRUS/

This was a retrospective study to evaluate the prevalence and impact o f hepatitis G virus (HGV) infection in hepatitis C virus (HCV)-positiv e drug addicts, according to the serological status of hepatitis B vir us (HBV) and human immunodeficiency virus (HIV) coinfection. Two hundr ed and thirty-five randomly selected intravenous drug addicted patient s (147 French, 88 Italian) were studied. All patients were positive fo r antibodies to HCV (anti-HCV), HGV RNA positivity was measured by rev erse transcriptase-polymerase chain reaction (RT-PCR). Comparisons of HCV RNA positivity rate, and biological and histopathological variable s, were made between HGV RNA-positive and negative patients, according to their HBV and HIV status. HGV prevalence was around 30% in both Fr ench and Italian groups. No clear association between HGV infection an d a particular HCV genotype was observed, The rate of HCV RNA positivi ty did not differ between HGV-positive and HGV-negative patients after stratification for hepatitis B surface antigen (HBsAg) and HIV positi vity, Histological severity of the underlying chronic hepatitis did no t differ according to the HGV status; however, in HIV-positive HBsAg-n egative patients, the hepatitis activity was moderately increased in H GV-positive patients. A striking negative influence of HBsAg positivit y 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 H BsAg-negative patients; similar significant results were observed in H IV-positive patients, although to a lesser extent, The underlying chro nic hepatitis was significantly more severe in HBsAg-positive than in HBsAg-negative HIV-negative patients. Hence, HGV infection is highly p revalent in anti-HCV positive drug addicts but the co-infection with H CV does not seem to influence HCV replication nor to worsen the underl ying chronic hepatitis, in HIV-negative patients at least, Reciprocal influence between HBV, HCV and HIV appears rather complex, HBsAg carri age seeming to exert per se a negative effect on HCV replication, part icularly in HIV-negative patients, suggesting that interactions betwee n hepatitis viruses should always be analysed in the light of HIV stat us.