The GB virus C/hepatitis G virus replicates in hepatocytes without causing liver disease in healthy blood donors.

Thirty-seven persons were identified with GB virus C (GBV-C) single infection by polymerase chain reaction screening of 1254 healthy blood donors. Of 33 donors who returned for clinical examination, 17 underwent liver biopsy. Clinical, biochemical, and histologic evaluation did not reveal any signs of liver disease. Liver biopsies of 15 donors were analyzed by in situ hybridization with GBV-C RNA probes and immunologic staining for the GBV-C envelope 2 protein. GBV-C replication was identified in the cytoplasm of hepatocytes of 10 (67%) donor livers but in none of 7 liver biopsies of chronic hepatitis B virus carriers negative for serum GBV-C RNA. Thus, there was no evidence of liver disease in GBV-C-infected healthy blood donors despite viral replication in hepatocytes.

A high prevalence of serum GB virus C/hepatitis G virus RNA in children with and without liver disease.

The role of GB virus C/hepatitis G virus (GBV-C/HGV) in adult and pediatric liver disease is unclear. We detected serum GBV-C/HGV RNA by reverse transcriptase polymerase chain reaction in 1 (3%) of 38 cholestatic infants, in 4 (4%) of 95 children without liver disease, and in none of 30 children with autoimmune hepatitis. One cholestatic infant had antibodies, presumably maternal, to GBV-C/HGV. Sequence analysis of a nonstructural 3 region fragment suggested that mother-to-infant transmission was the route of infection for the cholestatic infant. The four infected children without liver disease had normal liver function test results and lacked risk factors for bloodborne infections. Thus, the detection of GBV-C/HGV RNA among children with and without liver disease suggests that chronic GBV-C/ HGV infections may be established early in life, possibly by mother-to-infant transmission. This may explain in part the high prevalence of serum GBV-C/HGV RNA and antibodies in healthy adults.