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Comparative histologic features of liver biopsy specimens from patients coinfected with hepatitis G and C viruses with chronic hepatitis C virus alone: an age-, sex-, disease duration-, and transmission-matched controlled study of chronic hepatitis.

Hepatitis G virus (HGV) is a recently described, parenterally spread, positive-strand RNA virus of the Flaviviridae family. There is a high rate of HGV coinfection in patients with hepatitis C virus (HCV). Whether HGV can cause or is pathogenetically related to clinically apparent chronic liver disease, or whether HGV alters the course of hepatitis C in patients who are coinfected with both viruses is unknown. We studied 13 biopsy specimens from 11 patients coinfected with HGV and HCV and compared them with 15 biopsy specimens from a group of patients infected only with HCV who were matched for age, sex, disease duration, and transmission mode to characterize the histologic features of coinfected liver biopsy specimens and to look for any histologic features that might allow identification of coinfected patients. Three of the biopsy specimens from coinfected patients had a modified histologic activity index score of minimal chronic hepatitis, three of mild, two of mild/moderate, and five of moderate chronic hepatitis. Bile duct injury was absent in seven specimens, minimal in five, and mild in one. The biopsy specimens from patients who were coinfected with HGV and HCV had similar histologic features to the biopsy specimens of patients infected with HCV alone. There were no detectable histologic differences between the biopsy specimens from the two patient groups. The P values for the statistical comparisons confirmed this impression. In addition, no group of histologic features distinguished the coinfected patient group from the control group. Any suspicion that a clinician might have about the presence of HGV requires confirmation by reverse transcriptase-polymerase chain reaction testing of serum samples. Our results suggest that HGV most likely does not actively participate in the cytotoxic effects of chronic hepatitis or does so by a mechanism as yet undefined. Although HGV can cause chronic infection, the present study provides no evidence that it causes or contributes to chronic hepatitis.