Significance of coinfection with hepatitis G virus for chronic hepatitis C--a review of the literature
Rambusch, E.G.; Wedemeyer, H.; Tillmann, H.L.; Heringlake, S.; Manns, M.P.
Zeitschrift für Gastroenterologie 36(1): 41-53
1998
ISSN/ISBN: 0044-2771 PMID: 9531689 Document Number: 488999
The clinical significance of the recently discovered hepatitis C virus (HGV/GB virus C (GBV-C) is not conclusively clarified. The aim of this analysis was to evaluate the frequency of HGV/GBV-C coinfection at existing hepatitis C infection, the significance for the course of the liver disease, and its response to antiviral therapy. The literature available by medline and the PubMed Retrieval System as well as abstracts of recent German, European, and American conferences on liver diseases (GASL, EASL, ASSLU) concerning HCV/GBV-C-coinfection were analyzed. We identified 66 references with 5,388 patients suffering from HCV-infection. 941 (17.5%) were coinfected with GBV-C. Excluding some groups at risk (intravenous drug abusers, dialysis patients, patients after liver transplantation), the rate of coinfection varied significantly in respect to geography: 20.5% in European vs. 10.9% in Japan (p < 0.0001). Additionally, coinfection occurred in 38% of intravenous drug users. The studies showed that coinfection was related to the frequency of blood transfusions. Furthermore, the parenteral transmission route of GBV-C was generally confirmed. Overall GBV-C does not seem to have any negative influence on the course of HCV-related chronic liver disease or the development of chronicity of acute hepatitis C infection, nor does it have any influence on histology, transaminase-levels or response of HCV to antiviral therapy; GBV-C was shown to be sensitive to interferon-alpha with a relapse rate up to 53% comparable to HCV. There is no correlation between response of HCV and GBV-C to interferon. This analysis of the published data concerning coinfection of HCV and HGV/GBV-C revealed no influence of GBV-C on the course of HCV-related liver disease (clinical, biochemical, histological). GBV-C does not modify the response rate of HCV to interferon-alpha, but GBV-C is sensitive to interferon with high relapse rates.