Evaluate the relationship between polymorphisms of OAS1 gene and susceptibility to chronic hepatitis C with high resolution melting analysis

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Abstract

The aim of this was to investigate the relationship between single-nucleotide polymorphisms (SNPs) in the OAS1 gene and the susceptibility to chronic hepatitis C virus (HCV) infection in a population from the Liaoning Province of China. High resolution melt (HRM)-PCR analysis was conducted to examine three OAS1 SNPs: rs2660 G/A, rs10774671 G/A, and rs3741981 G/A in 298 chronic HCV-infected patients and in 305 healthy controls and to identify a relationship between SNP genotype and susceptibility to chronic HCV infection using a case-control study design. These three OAS1 SNPs were in strong linkage disequilibrium (rs2660 vs. rs10774671: |D'|=1.000, r 2 =1.000; rs2660/rs10774671 vs. rs3741981: |D'|=0.938, r 2 =0.569). The frequency of AG + GG genotypes in both rs2660 and rs10774671 and the AA + AG genotype in rs3741981 was significantly higher among chronic HCV-infected patients than among control (P < 0.001); the A allele in all three SNPs was found more frequently in the chronic HCV-infected group than in the control group (rs2660 and rs10774671: P = 0.02; rs3741981: P < 0.001). Moreover, individuals carrying the A allele in these SNPs exhibited an increased risk for chronic HCV infection (rs2660 and rs10774671: OR = 1.356 [1.051-1.749]; rs3741981: 1.363 [1.085-1.712]). The haplotype created by the G allele at both rs2660 and rs10774671 and the A allele at rs3741981 increased the risk of chronic HCV infection by 3.394-fold (95 % CI 1.406-8.201). Our results identify OAS1 SNP rs2660, rs10774671, and rs3741981 as genetic risk factors for chronic HCV infection. Polymorphisms of the OAS1 gene might affect the susceptibility to chronic infection with HCV. © 2012 Springer-Verlag.

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APA

Zhao, Y., Kang, H., Ji, Y., & Chen, X. (2013). Evaluate the relationship between polymorphisms of OAS1 gene and susceptibility to chronic hepatitis C with high resolution melting analysis. Clinical and Experimental Medicine, 13(3), 171–176. https://doi.org/10.1007/s10238-012-0193-6

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