title: Effects of hepatitis G virus coinfection on severity of hepatitis C: relationship to risk factors and response to interferon treatment.
abstract: The aims of the present study were to identify characteristics that are more often associated with hepatitis G virus (HGV) coinfection in Australian patients infected with the hepatitis C virus (HCV) and to investigate the effects of HGV on the histological and functional severity of chronic hepatitis C. Serum samples from 209 patients with chronic hepatitis C were tested for HGV-RNA using single-round reverse transcriptase-polymerase chain reaction to primers directed at the NS5 region of the HGV genome. Hepatitis G virus RNA was detected in 40 cases (19%). Hepatitis G virus-coinfected patients tended to be younger and parenteral risks could be identified in all but six. Although country of birth did not differ significantly between the coinfected and HCV-alone groups, HGV-positive patients appeared to be less likely to have originated from Asia. On logistic regression analysis, HCV genotype 3a was found in a significantly higher proportion of patients with HGV coinfection than other genotypes (P < 0.01). Liver histology and response to interferon were similar in the HGV-coinfected and HCV-alone groups and liver-related complications appeared to occur less frequently in patients with both HGV and HCV. On univariate analysis, antipyrine clearance was found to be higher in the coinfected group (P < 0.05), implying better preservation of hepatic metabolic function, but this difference was lost when adjusted for HCV genotype. In conclusion, coinfection with HGV was more commonly associated with HCV genotype 3a, a genotype associated with injection drug use in younger patients. However, the presence of HGV coinfection did not adversely affect liver disease or the response to interferon treatment in patients with chronic hepatitis C.
authors.affiliation: Department of Medicine, University of Sydney, Westmead Hospital, New South Wales, Australia.
authors.forename: R
authors.initials: R
authors.lastname: Lin
authors.forename: U
authors.initials: U
authors.lastname: Dutta
authors.forename: S
authors.initials: S
authors.lastname: Kaba
authors.forename: J
authors.initials: J
authors.lastname: Kench
authors.forename: E
authors.initials: E
authors.lastname: Crewe
authors.forename: S
authors.initials: S
authors.lastname: Coverdale
authors.forename: K
authors.initials: K
authors.lastname: Byth
authors.forename: C
authors.initials: C
authors.lastname: Liddle
authors.forename: G C
authors.initials: GC
authors.lastname: Farrell
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D001315:Australia; D015415:Biomarkers / Q000097:blood; D005260:Female; D018067:Flaviviridae / Q000235:genetics / Q000302:isolation & purification*; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification*; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology / Q000821:virology*; D006525:Hepatitis, Viral, Human / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology / Q000821:virology*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins