Hepatitis C virus genotypes, reactivity to recombinant immunoblot assay 2 antigens and liver disease

Abstract

To clarify the relationship between hepatitis C virus (HCV) genotypes and liver disease, we typed HCV genomes in the sera of 151 blood donors, 180 patients with type C chronic liver disease (CLD), and 30 haemophiliacs residing in Hiroshima, Japan. All of the subjects were positive for anti-HCV and HCV-RNA, and were examined for seroreactivity to HCV-specific antigens. The HCV genotypes were determined by polymerase chain reaction (PCR) with type-specific primers deduced from the putative core region of the HCV genome. Significantly more (P< 0.001) type II HCV was found in the samples from the CLD patients (80%) than in those from the blood donors (55%). Significantly more (P< 0.001) type III HCV was found in the samples from the blood donors (29.1%) than in those from the CLD patients (11.7%). There was no significant difference in the distribution of the HCV types among the patients with chronic active hepatitis, liver cirrhosis, and hepatocellular carcinoma. A four-antigen recombinant immunoblot assay (RIBA-2) assay was used to compare the serum samples for their reactivity to a range of structural and nonstructural peptides specific for HCV (5–1–1, C100-3, C33c, and C22-3). The frequency of serop-ositivity to 5–1–1 and C100-3 was significantly higher (P < 0.001) in type II HCV-infected blood donors than in type III HCV-infected donors (68.2% and 65.9% vs. 4.5% and 22.7%, respectively). Among the type III HCV-infected individuals, the CLD patients had a significantly higher (P<0.01) frequency of seropositivity to 5–1–1 than the blood donors (33.3% vs. 4.5%). These results suggest that type II HCV is more likely than type III HCV to induce clinical disease, and further, that the difference in the extent of synthesis of the viral protein (5–1–1) between these types may play a role in the pathogenicity of HCV.