Hepatitis G virus biology, epidemiology, and clinical manifestations: Implications for blood safety.

Abstract

Hepatitis G virus (HGV), also called GBV-C, is a single positive-standard RNA virus belonging to the Flaviviridae family. In 50% to 75% of infections, HGV is cleared with plasma RNA disappearing as anti-E2 becomes detectable; in other cases, HGV infection becomes chronic. The prevalence of HGV RNA in blood donors ranges from 1% to 4%, and the rate of anti-E2, indicating resolved infection, ranges from 3% to 14%. HGV is transmitted by transfusion of blood components and has been transmitted by nonvirally inactivated factor VIII concentrate. Despite extensive study, HGV has not been identified as a causative agent of any type of liver disease or any other known clinical condition. Molecular biology data show a lack of hepatotropism; preliminary data indicate that the site of HGV replication may be in mononuclear cells in bone marrow or spleen but not in peripheral blood or lymph nodes. The combined clinical and laboratory data strongly support the contention that HGV is not a hepatotropic virus and that this virus was inappropriately named hepatitis G. Because the data do not indicate any pathologic effects of HGV, it is not appropriate to screen the blood supply for HGV RNA.