Abstract
Interleukin-17 (IL-17) can accelerate the release of many pro-inflammatory cytokines. The purpose of our study was to investigate the potential association between polymorphisms in the IL-17 gene and susceptibility to hepatitis B virus (HBV) infection in the Han Chinese population. We recruited 596 HBV-infected patients and 612 ethnically matched controls, who were then genotyped for the IL-17A and IL-17F polymorphisms, rs2275913 and rs763780, respectively, by using TaqMan probe-based real-time polymerase chain reaction. The frequencies of the alleles and genotypes in patients and controls were compared by the χ2 test. Statistically significant differences in genotypic and allelic frequencies were revealed at both polymorphic sites between HBV-positive patients and controls (rs2275913: genotype χ2 = 37.74, p < 0.001 and allele χ2 = 22.17, p < 0.001, odds ratio [OR] = 0.654, 95% confidence interval [CI] = 0.548-0.781. rs763780: genotype χ2 = 19.80, p < 0.001 and allele χ2 = 18.78, p < 0.001, OR = 0.507, 95% CI = 0.371-0.692). These results indicate that the IL-17A rs2275913 and IL-17F rs763780 polymorphisms are associated with HBV infection in the Han Chinese population. We conclude that possession of the GG genotype and the G allele at rs2275913, and the TT genotype and the T allele at rs763780 might increase the risk of HBV infection. Larger-scale, multiracial studies are necessary to evaluate the role of IL-17 polymorphisms in relation to an enhanced risk of HBV infection.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.