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 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) coinfection. 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.
Thiers
V
V
Centre de Biologie Moléculaire Spécialisée, Institut Pasteur, Paris, France.
Pol
S
S
Persico
T
T
Carnot
F
F
Zylberberg
H
H
Berthelot
P
P
Bréchot
C
C
Nalpas
B
B
D000328:Adult; D005260:Female; D018067:Flaviviridae / Q000235:genetics; D005838:Genotype; D006678:HIV / Q000276:immunology; D015658:HIV Infections / Q000150:complications* / Q000276:immunology; D006509:Hepatitis B / Q000150:complications / Q000276:immunology; D006510:Hepatitis B Antibodies / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000254:growth & development / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000097:blood; D019698:Hepatitis C, Chronic / Q000150:complications / Q000276:immunology; D006525:Hepatitis, Viral, Human / Q000150:complications* / Q000276:immunology; D006801:Humans; D008297:Male; D015995:Prevalence; D012367:RNA, Viral / Q000097:blood / Q000302:isolation & purification; D012189:Retrospective Studies
D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D018937:Hepatitis C Antibodies; D012367:RNA, Viral