title: Response to interferon in chronic hepatitis C due to mixed genotype infection.
abstract: We examined the response to interferon (IFN) in patients with chronic hepatitis C (CHC) due to two different genotypes of hepatitis C virus (HCV) infection. Among 64 CHC patients studied, one (2%) had HCV-RNA genotype I, 36 (56%) had genotype II, 19 (30%) had genotype III, 2 (3%) had genotype IV and 6 (9%) had both genotypes II and III. There was no significant difference in age, sex, history of blood transfusion and liver histology among patients with genotypes II, III and II + III. The HCV-RNA titre of genotype II patients was significantly higher than that of genotype III patients (P < 0.05). However, there was no significant difference in the HCV-RNA titre between genotype II + III and the other groups. The complete response rate achieved with IFN therapy was significantly higher in genotype III patients (74%) than in genotype II patients (17%; P < 0.01). Of the six patients with genotype II + III, a complete response to IFN was only achieved by two patients (33%), both of whom had a low HCV-RNA titre ( < or = 10(4.5) copies/mL) and HCV serotype 2. The remaining four patients had HCV serotype 1 and three of the patients had a high HCV-RNA titre ( > or = 10(5) copies/mL). The HCV genotype III was lost in two patients after IFN therapy. These data suggest that HCV-RNA titre and HCV serotype are important factors for predicting the efficacy of IFN therapy in patients with mixed genotype infection and show direct evidence of higher susceptibility towards CHC of patients with genotype III than genotype II.
authors.affiliation: Third Department of Internal Medicine, Ehime University School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Horiike
authors.forename: T
authors.initials: T
authors.lastname: Masumoto
authors.forename: K
authors.initials: K
authors.lastname: Michitaka
authors.forename: K
authors.initials: K
authors.lastname: Kurose
authors.forename: S M
authors.initials: SM
authors.lastname: Akbar
authors.forename: M
authors.initials: M
authors.lastname: Onji
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000595:Amino Acid Sequence; D001483:Base Sequence; D002908:Chronic Disease; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics*; D006526:Hepatitis C / Q000628:therapy* / Q000821:virology*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D015335:Molecular Probes / Q000235:genetics; D008969:Molecular Sequence Data; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins; D012703:Serotyping
chemical_list: D000077190:Interferon alpha-2; D016898:Interferon-alpha; D015335:Molecular Probes; D012367:RNA, Viral; D011994:Recombinant Proteins