COMPARATIVE HISTOLOGIC FEATURES OF LIVER-BIOPSY SPECIMENS FROM PATIENTS COINFECTED WITH HEPATITIS-G-VIRUSES AND HEPATITIS-C-VIRUSES WITH CHRONIC HEPATITIS-C-VIRUS ALONE - AN AGE, SEX, DISEASE DURATION, AND TRANSMISSION MATCHED CONTROLLED STUDY OF CHRONIC HEPATITIS
Ns. Goldstein et al., COMPARATIVE HISTOLOGIC FEATURES OF LIVER-BIOPSY SPECIMENS FROM PATIENTS COINFECTED WITH HEPATITIS-G-VIRUSES AND HEPATITIS-C-VIRUSES WITH CHRONIC HEPATITIS-C-VIRUS ALONE - AN AGE, SEX, DISEASE DURATION, AND TRANSMISSION MATCHED CONTROLLED STUDY OF CHRONIC HEPATITIS, American journal of clinical pathology, 108(6), 1997, pp. 625-632
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). Whet
her HGV can cause or is pathogenetically related to clinically apparen
t chronic liver disease, or whether HGV alters the course of hepatitis
C in patients who are coinfected with both viruses is unknown. We stu
died 13 biopsy specimens from 11 patients coinfected with HGV and HCV
and compared them with 15 biopsy specimens from a group of patients in
fected only with HCV who were matched for age, sex, disease duration,
and transmission mode to characterize the histologic features of coinf
ected liver biopsy specimens and to look for any histologic features t
hat might allow identification of coinfected patients. Three of the bi
opsy specimens from coinfected patients had a modified histologic acti
vity index score of minimal chronic hepatitis, three of mild, two of m
ild/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 ha
d similar histologic features to the biopsy specimens of patients infe
cted with HCV alone. There were no detectable histologic differences b
etween 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 ha
ve about the presence of HGV requires confirmation by reverse transcri
ptase-polymerase chain reaction testing of serum samples. Our results
suggest that HGV most likely does not actively participate in the cyto
toxic effects of chronic hepatitis or does so by a mechanism as yet un
defined. Although HGV can cause chronic infection, the present study p
rovides no evidence that it causes or contributes to chronic hepatitis
.