GB virus-C/hepatitis G virus infection in Taiwan: a virus that fails to cause a disease?

Recently, an RNA virus designated GB virus-C or hepatitis G virus (GBV-C/HGV) was identified; however, its clinical significance remains uncertain. This discovery prompted us to investigate the virological, epidemiological and clinical implications of GBV-C/HGV infection in Taiwan where chronic liver diseases and liver cancer are endemic. Our results showed that genetic heterogeneity of GBV-C/HGV isolates exists, and primers from the highly conserved 5' untranslated region of viral genome can efficiently detect GBV-C/HGV RNA. Epidemiological surveys showed that GBV-C/HGV infection is common in high-risk groups in Taiwan, and its coinfection does not aggravate the course of chronic hepatitis B or C. A prospective study of transfusion-transmitted GBV-C/HGV infection also showed GBV-C/HGV does not cause classic hepatitis in most patients. In addition, GBV-C/HGV plays a minimal role in causing fulminant hepatitis. Like hepatitis C virus, sexual transmission of GBV-C/HGV exists. The risk increases with prolonged duration of exposure. In addition, high-titered maternal viremia and mode of delivery are associated with the mother-to-infant transmission of GBV-C/HGV. Interestingly, we found that GBV-C/HGV exerts no suppression on levels of chronic hepatitis B or hepatitis C viremia, and GBV-C/HGV responds to interferon; however, ribavirin plus interferon does not induce a higher sustained response. As to the replication sites of GBV-C/HGV, our preliminary results showed liver and peripheral blood mononuclear cells are not the major sites for GBV-C/HGV replication, and thus GBV-C/HGV is not a primary hepatotropic virus. In conclusion, transfusion and exchange of body fluids indeed can transmit GBV-C/HGV; however, current lines of evidence suggest that GBV-C/HGV fails to cause a disease.