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/HG V) was identified; however, its clinical significance remains uncertain. Th is discovery prompted us to investigate the virological, epidemiological an d clinical implications of GBV-C/HGV infection in Taiwan where chronic live r diseases and liver cancer are endemic. Our results showed that genetic he terogeneity of GBV-C/HGV isolates exists, and primers from the highly conse rved 5' untranslated region of viral genome can efficiently detect GBV-C/HG V RNA. Epidemiological surveys showed that GBV-C/HGV infection is common in high-risk groups in Taiwan, and its coinfection does not aggravate the cou rse of chronic hepatitis B or C. A prospective study of transfusion-transmi tted GBV-C/HGV infection also showed GBV-C/HGV does not cause classic hepat itis in most patients. In addition, GBV-C/HGV plays a minimal role in causi ng fulminant hepatitis. Like hepatitis C virus, sexual transmission of GBV- C/HGV exists. The risk increases with prolonged duration of exposure. In ad dition, high-titered maternal viremia and mode of delivery are associated w ith 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 h epatitis C viremia, and GBV-C/HGV responds to interferon; however, ribaviri n plus interferon does not induce a higher sustained response. As to the re plication sites of GBV-C/HGV, our preliminary results showed liver and peri pheral blood mononuclear cells are not the major sites for GBV-C/HGV replic ation, and thus GBV-C/HGV is not a primary hepatotropic virus. In conclusio n, transfusion and exchange of body fluids indeed can transmit GBV-C/HGV; h owever, current lines of evidence suggest that GBV-C/HGV fails to cause a d isease.