Top

Published in:

01-08-2013 | Original Article

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

Authors: Yan Zhao, Hui Kang, Yangtang Ji, Xin Chen

Published in: Clinical and Experimental Medicine | Issue 3/2013

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.

Liew M, Pryor R, Palais R, Meadows C, Erali M, Lyon E, Wittwer C (2004) Genotyping of single-nucleotide polymorphisms by high-resolution melting of small amplicons. Clin Chem 50:1156–1164PubMedCrossRef

Justesen J, Hartmann R, Kjeldgaard NO (2000) Gene structure and function of the 2′-5′-oligoadenylate synthetase family. Cell Mol Life Sci 57:1593–1612PubMedCrossRef

Hartmann R, Justesen J, Sarkar SN, Sen GC, Yee VC (2003) Crystal structure of the 2′-specific and double-stranded RNA-activated interferon-induced antiviral protein 2′-5′-oligoadenylate synthetase. Mol Cell 12:1173–1185PubMedCrossRef

Sadler AJ, Williams BR (2008) Interferon-inducible antiviral effectors. Nat Rev Immunol 8:559–568PubMedCrossRef

Lin RJ, Yu HP, Chang BL, Tang WC, Liao CL, Lin YL (2009) Distinct antiviral roles for human 2′, 5′-oligoadenylate synthetase family members against dengue virus infection. J Immunol 183:8035–8043PubMedCrossRef

Silverman RH (2007) Viral encounters with 2′, 5′-oligoadenylate synthetase and RNase L during the interferon antiviral response. J Virol 81:12720–12729PubMedCrossRef

Chen LB, Peng XM, Cao H, Zhang YF, Xu QH, Gao ZL (2009) Relationship between SNP rs10774671 on OAS-1 gene and spontaneous HBeAg seroconversion in chronic HBV infection. Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi 23:35–37PubMed

Fedetz M, Matesanz F, Caro-Maldonado A, Fernandez O, Tamayo JA, Guerrero M, Delgado C, Lopez-Guerrero JA, Alcina A (2006) OAS1 gene haplotype confers susceptibility to multiple sclerosis. Tissue Antigens 68:446–449PubMedCrossRef

Li CZ, Kato N, Chang JH, Muroyama R, Shao RX, Dharel N, Sermsathanasawadi R, Kawabe T, Omata M (2009) Polymorphism of OAS-1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication. Liver Int 29:1413–1421PubMedCrossRef

10.

Hamano E, Hijikata M, Itoyama S, Quy T, Phi NC, Long HT, Ha LD, Ban VV, Matsushita I, Yanai H, Kirikae F, Kirikae T, Kuratsuji T, Sasazuki T, Keicho N (2005) Polymorphisms of interferon-inducible genes OAS-1 and MxA associated with SARS in the Vietnamese population. Biochem Biophys Res Commun 329:1234–1239PubMedCrossRef

11.

Knapp S, Yee LJ, Frodsham AJ, Hennig BJ, Hellier S, Zhang L, Wright M, Chiaramonte M, Graves M, Thomas HC, Hill AV, Thursz MR (2003) Polymorphisms in interferon-induced genes and the outcome of hepatitis C virus infection: roles of MxA, OAS-1 and PKR. Genes Immun 4:411–419PubMedCrossRef

12.

He J, Feng D, de Vlas SJ, Wang H, Fontanet A, Zhang P, Plancoulaine S, Tang F, Zhan L, Yang H, Wang T, Richardus JH, Habbema JD, Cao W (2006) Association of SARS susceptibility with single nucleic acid polymorphisms of OAS1 and MxA genes: a case-control study. BMC Infect Dis 6:106PubMedCrossRef

13.

Lim JK, Lisco A, McDermott DH, Huynh L, Ward JM, Johnson B, Johnson H, Pape J, Foster GA, Krysztof D, Follmann D, Stramer SL, Margolis LB, Murphy PM (2009) Genetic variation in OAS1 is a risk factor for initial infection with West Nile virus in man. PLoS Pathog 5:e1000321PubMedCrossRef

14.

Field LL, Bonnevie-Nielsen V, Pociot F, Lu S, Nielsen TB, Beck-Nielsen H (2005) OAS1 splice site polymorphism controlling antiviral enzyme activity influences susceptibility to type 1 diabetes. Diabetes 54:1588–1591PubMedCrossRef

15.

Smyth DJ, Cooper JD, Lowe CE, Nutland S, Walker NM, Clayton DG, Todd JA (2006) No evidence for association of OAS1 with type 1 diabetes in unaffected siblings or type 1 diabetic cases. Diabetes 55:1525–1528PubMedCrossRef

16.

Tessier MC, Qu HQ, Frechette R, Bacot F, Grabs R, Taback SP, Lawson ML, Kirsch SE, Hudson TJ, Polychronakos C (2006) Type 1 diabetes and the OAS gene cluster: association with splicing polymorphism or haplotype? J Med Genet 43:129–132PubMedCrossRef

17.

Howson JM, Walker NM, Smyth DJ, Todd JA, Type IDG.C. (2009) Analysis of 19 genes for association with type I diabetes in the Type I Diabetes Genetics Consortium families. Genes Immun 10(suppl 1):S74–S84PubMedCrossRef

18.

Qu HQ, Polychronakos C, Type IDGC (2009) Reassessment of the type I diabetes association of the OAS1 locus. Genes Immun 10(suppl 1):S69–S73PubMedCrossRef

19.

Bonnevie-Nielsen V, Field LL, Lu S, Zheng DJ, Li M, Martensen PM, Nielsen TB, Beck-Nielsen H, Lau YL, Pociot F (2005) Variation in antiviral 2′, 5′-oligoadenylate synthetase (2′5′AS) enzyme activity is controlled by a single-nucleotide polymorphism at a splice-acceptor site in the OAS1 gene. Am J Hum Genet 76:623–633PubMedCrossRef

20.

Gatignol A, Buckler-White A, Berkhout B, Jeang KT (1991) Characterization of a human TAR RNA-binding protein that activates the HIV-1 LTR. Science 251:1597–1600PubMedCrossRef

21.

Green SR, Mathews MB (1992) Two RNA-binding motifs in the double-stranded RNA-activated protein kinase, DAI. Genes Dev 6:2478–2490PubMedCrossRef

22.

Krovat BC, Jantsch MF (1996) Comparative mutational analysis of the double-stranded RNA binding domains of Xenopus laevis RNA-binding protein A. J Biol Chem 271:28112–28119PubMedCrossRef

23.

Huang Q, Fu YX, Boerwinkle E (2003) Comparison of strategies for selecting single nucleotide polymorphisms for case/control association studies. Hum Genet 113:253–257PubMedCrossRef

24.

Lautier C, El Mkadem SA, Renard E, Brun JF, Gris JC, Bringer J, Grigorescu F (2003) Complex haplotypes of IRS2 gene are associated with severe obesity and reveal heterogeneity in the effect of Gly1057Asp mutation. Hum Genet 113:34–43PubMed

Title: Evaluate the relationship between polymorphisms of OAS1 gene and susceptibility to chronic hepatitis C with high resolution melting analysis
Authors: Yan Zhao
Hui Kang
Yangtang Ji
Xin Chen
Publication date: 01-08-2013
Publisher: Springer Milan
Published in: Clinical and Experimental Medicine / Issue 3/2013
Print ISSN: 1591-8890
Electronic ISSN: 1591-9528
DOI: https://doi.org/10.1007/s10238-012-0193-6

Live Webinar | 27-06-2024 | 18:00 (CEST)

Keynote webinar | Spotlight on medication adherence

Reserve your place

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

WHO estimates that half of all patients worldwide are non-adherent to their prescribed medication. The consequences of poor adherence can be catastrophic, on both the individual and population level.

Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.

Prof. Kevin Dolgin

Prof. Florian Limbourg

Prof. Anoop Chauhan

Developed by: Springer Medicine

Obesity Clinical Trial Summary

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Abstract

Please log in to get access to this content

Other articles of this Issue 3/2013

Granulomatous skin lesions in a renal transplant patient

Chronic spontaneous urticaria: an autoimmune disease? A revision of the literature

Resveratrol prevents TNFα-induced suppression of adiponectin expression via PPARγ activation in 3T3-L1 adipocytes

CXCL12, CXCR4 and IFNγ genes expression: implications for proinflammatory microenvironment of breast cancer

The involvement of Notch signaling in melanoma vasculogenic mimicry

Negative effect of immunosuppressive therapy in the performance of the QuantiFERON Gold In-Tube test in patients with immune-mediated inflammatory diseases

Keynote webinar | Spotlight on medication adherence

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

At a glance: The STEP trials