Eighty-two patients with bleeding disorders registered with our centre
were screened for infection with hepatitis G virus (HGV). 80 patients
were positive for hepatitis C (HCV) antibodies, 66 of whom (83%) were
HCV PCR positive. 11 patients (13%) were HGV RNA-positive, a similar
prevalence rate to that of other studies of patients with bleeding dis
orders who received factor concentrates prior to the introduction of v
iral inactivation procedures. There was no significant difference in h
istological activity index (HAI) between the 10 HGV RNA-positive and t
he 31 HGV RNA-negative patients who underwent liver biopsy for assessm
ent of HCV infection (median HAI scores 5.5, range 2-10 and four, rang
e 0-10 respectively, P=0.07). One patient in each group had establishe
d cirrhosis. In patients who underwent HCV quantitation there was no s
ignificant difference in HCV viral titre between HGV RNA-positive and
negative patients (median HCV titre in HGV RNA-positive patients 2.10x
10(5) DNA copies/ml (n = 8) range 4.17x10(2) to 4.17x10(6), median HCV
titre in HGV RNA-negative patients 3.33x10(5) (n = 31) range 1.00x10(
3) to 6.67x10(6), P=0.68). In this study there was no evidence that in
dividuals co-infected with HGV and HCV have more severe liver disease
than those infected with HCV alone.