1. Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication
- Author
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Jin-Hai Chang, Takao Kawabe, Radsamee Sermsathanasawadi, Run-Xuan Shao, Ryosuke Muroyama, Narayan Dharel, Naoya Kato, Masao Omata, and Chang-Zheng Li
- Subjects
Adult ,Liver Cirrhosis ,Male ,Cirrhosis ,Genotype ,Hepatitis C virus ,SNP ,Single-nucleotide polymorphism ,Biology ,medicine.disease_cause ,Virus Replication ,Polymorphism, Single Nucleotide ,Clinical Studies ,medicine ,2',5'-Oligoadenylate Synthetase ,Humans ,JFH1 ,Allele ,Genotyping ,Aged ,Aged, 80 and over ,Hepatology ,cirrhosis ,fibrosis ,Hepatitis C ,Hepatitis C, Chronic ,Middle Aged ,medicine.disease ,Virology ,Viral replication ,Disease Progression ,Female ,Interferons ,replicon - Abstract
Background: Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′-5′-oligoadenylate synthetase 1 (OAS-1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease. Aim: To evaluate single nucleotide polymorphisms (SNPs) of OAS-1 and its relationship with the disease status of HCV infection. Methods: Six SNPs of OAS-1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS-1-expression plasmids mimicking the clinical-related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full-length genome, JFH1, and HCV replication after transfection was compared. Results: Patients with genotypes A/A, A/G and G/G of an SNP of OAS-1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (P
- Published
- 2009