title: Detection of three types of hepatitis C virus in blood donors: investigation of type-specific differences in serologic reactivity and rate of alanine aminotransferase abnormalities.
abstract: The serologic reactivity and epidemiology associated with different hepatitis C virus (HCV) variants were investigated in a cohort of 113 anti-HCV-positive donors. In Scotland, HCV type 1 accounted for one-half of all infections; 40 percent of subjects were infected with HCV type 3, and the remainder were infected with type 2. Reactivity with the NS-4-encoded antigens in the first-generation anti-c100 assay was absent in 68 percent of donors infected with types 2 and 3, as compared with 10 percent for those infected with type 1. Even when combined with surrogate marker testing, first-generation tests would have failed to detect 12 percent of HCV-infected blood donors. The age distribution, incidence of past infection with hepatitis B virus, and reported risk factors were similar in donors infected with types 1 and 3 (mean ages were 31.9 and 29.9; 18 and 17.5% were positive for antibody to hepatitis B core antigen; and 47 and 48% had past intravenous drug abuse). However, the distributions of alanine aminotransferase levels were significantly different in those infected with type 3 (abnormally raised in 83%) and those infected with type 1 (55% abnormal alanine aminotransferase; p < 0.05) or type 2 (60%; p < 0.01) and those who were nonviremic (8%; p < 0.0001). These data suggest that HCV type 1 is the most common HCV infection in blood donors and that infection with HCV type 3 may be associated with more severe liver disease, because of more recent infection or because of a greater inherent pathogenicity of type 3 variants.
authors.affiliation: Edinburgh and South East Scotland Blood Transfusion Service.
authors.forename: F
authors.initials: F
authors.lastname: McOmish
authors.forename: S W
authors.initials: SW
authors.lastname: Chan
authors.forename: B C
authors.initials: BC
authors.lastname: Dow
authors.forename: J
authors.initials: J
authors.lastname: Gillon
authors.forename: W D
authors.initials: WD
authors.lastname: Frame
authors.forename: R J
authors.initials: RJ
authors.lastname: Crawford
authors.forename: P L
authors.initials: PL
authors.lastname: Yap
authors.forename: E A
authors.initials: EA
authors.lastname: Follett
authors.forename: P
authors.initials: P
authors.lastname: Simmonds
mesh_terms: D000410:Alanine Transaminase / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001782:Blood Donors; D016174:Hepacivirus / Q000145:classification / Q000235:genetics / Q000302:isolation & purification*; D006508:Hepatitis Antibodies / Q000097:blood*; D006526:Hepatitis C / Q000097:blood* / Q000453:epidemiology / Q000635:transmission; D018937:Hepatitis C Antibodies; D006801:Humans; D009660:Northern Ireland / Q000453:epidemiology; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D012367:RNA, Viral / Q000097:blood / Q000235:genetics / Q000302:isolation & purification; D012606:Scotland / Q000453:epidemiology; D015819:Substance Abuse, Intravenous / Q000097:blood
chemical_list: D015415:Biomarkers; D006508:Hepatitis Antibodies; D018937:Hepatitis C Antibodies; D012367:RNA, Viral; D000410:Alanine Transaminase