Hepatitis G (HGV) is a flavivirus, which shares about 27 – 40% sequence homology with HCV (117). HGV is identical to the “GB-C” agent, originally found in a surgeon with hepatitis and later identified in animals to be different from hepatitis viruses A, B, C, D and E, respectively. Studies on post transfusion hepatitis in HGV RNA-positive blood donors, and in community acquired acute hepatitis have suggested that HGV is not an important cause of chronic liver disease (118,119).Some patients who acquired hepatitis G from transfusion have developed a mild transient aminotransferase elevation that resolves spontaneously (120). Although the virus may persist, it appears that chronic liver disease do not ensue. Further, the liver is not the primary site of HGV replication (121). There is a high prevalence of HGV in blood donors, perhaps in the order of 1-2%. Fulminant hepatitis is rare. HGV is transmitted by intravenous and sexual routes and perhaps also via perinatal transmission. Its presence in liver transplant recipients does not affect the outcome of the disease (122). Routine screening of blood donors or wide spread testing for HGV is not recommended. Diagnosis requires virologic methods based on PCR or serologic assays using the E2 antibody. Neither of these is readily available.

 
TRANSFUSION TRANSMITTED VIRUS