The hepatitis G virus (HGV) is a newly discovered member of the Flaviviridae family that has approximately 25 percent homology with hepatitis C virus (HCV). Its clinical significance is unknown. We have studied HGV and its relation to blood transfusion risk. HGV was found in approximately 1.5 percent of the donor population. It was shown to be transfusion-transmitted by demonstrating the acute appearance of HGV RNA following transfusion and by linkage between HGV positive donors and infected recipients. HGV can establish persistent infection, but the majority (perhaps 80 percent) clear the virus over time. Although 3 of 13 patients (23 percent) with non-ABC transfusion-associated hepatitis had acute HGV infection, the causal role of HGV in these cases is not clear because there was no definite temporal relationship between HGV RNA level and alanine aminotransferase elevations. Overall, of 35 observed and 84 projected HGV infections, only 4 percent occurred in patients with hepatitis unrelated to HCV, but as indicated above the hepatitis was probably not due to HGV; 89 percent of HGV infections occurred in recipients with no evidence of hepatitis. Among patients coinfected with HGV and HCV, it was shown that HGV did not worsen the course coexistent hepatitis C. Similarly, we have studied HGV in renal dialysis patients, hemophiliacs, intravenous drug users, and patients with acute and chronic non-ABC hepatitis. Although the prevalence of HGV is very high among parenterally exposed individuals (10 to 20 percent), there is no association with liver disease in these HGV-infected populations. Studies of antibody to the HGV envelope (anti-E2) have shown that HGV RNA and anti-E2 are mutually exclusive and that the latter is a marker of recovery.
