A case-control study on association between OAS1 polymorphism and susceptibility to spontaneous preterm birth and preterm premature rupture of membranes
YANG Xiao1, ZHANG Xiao-Ai2, WU Zhi-Hao3, PENG Wei1, ZHU Li-Na1, WANG Yan1
Developmental Biology Laboratory, Baiyi Children's Hospital Affiliated to Beijing Military General Hospital, Beijing 100700, China
Abstract：Objective To investigate the association between the genetic polymorphism of 2',5'-oligoadenylate synthetase 1 (OAS1) and susceptibility to spontaneous preterm birth (SPTB) and preterm premature rupture of membranes (PPROM).Methods The case-control study consisted of 599 preterm infants including 171 cases of PPROM, and 673 full-term infants without maternal histories of SPTB and PPROM as controls. The single nucleotide polymorphism (SNP) at OAS1 intron 5, rs10774671, was analyzed by polymerase chain reaction-restriction fragment length polymorphism.Results No significant differences were observed between the case and control groups in the frequencies of genotypes (AA, GA, and GG) and alleles (A and G) of OAS1 rs10774671. When the case group was divided into two subgroups with or without PPROM, no significant differences in the genotype and allele frequencies were found between each subgroup and the control group. When the case group was divided into three subgroups with different gestational ages at SPTB, no significant differences in the genotype and allele frequencies were detected between each subgroup and the control group.Conclusions No association is identified between OAS1 SNP and susceptibility to SPTB and PPROM.
YANG Xiao,ZHANG Xiao-Ai,WU Zhi-Hao et al. A case-control study on association between OAS1 polymorphism and susceptibility to spontaneous preterm birth and preterm premature rupture of membranes[J]. CJCP, 2015, 17(9): 898-902.
Bhat G, Peltier MR, Syed TA, et al. Fetal membrane biomarker network diversity and disease functions induced by intraamniotic pathogens[J]. Am J Reprod Immunol, 2013, 69(2):124-133.
[2]
Varner MW, Esplin MS. Current understanding of genetic factors in preterm birth[J]. BJOG, 2005, 112 (Suppl 1):28-31.
[3]
Yilmaz Y, Verdi H, Taneri A, et al. Maternal-f et al proinflammatory cytokine gene polymorphism and preterm birth[J]. Dna Cell Biol, 2012, 31(1):92-97.
[4]
Macones GA, Parry S, Elkousy M, et al. A polymorphism in the promoter region of TNF and bacterial vaginosis:preliminary evidence of gene-environment interaction in the etiology of spontaneous preterm birth[J]. Am J Obstet Gynecol, 2004, 190(6):1504-1508.
[5]
Wang Y, Zhang XA, Yang X, et al. A MCP-1 promoter polymorphism at G-2518A is associated with spontaneous preterm birth[J]. Mol Genet Genomics, 2015, 290(1):289-296.
[6]
Wang Y, Yang X, Zheng Y, et al. The SEPS1 G-105A polymorphism is associated with risk of spontaneous preterm birth in a Chinese population[J]. PLoS One, 2013, 8(6):e65657.
[7]
Haralambieva IH, Dhiman N, Ovsyannikova I G, et al. 2'-5'-Oligoadenylate synthetase single-nucleotide polymorphisms and haplotypes are associated with variations in immune responses to rubella vaccine[J]. Hum Immunol, 2010, 71(4):383-391.
[8]
Justesen J, Hartmann R, Kjeldgaard NO. Gene structure and function of the 2'-5'-oligoadenylate synthetase family[J]. Cell Mol Life Sci, 2000, 57(11):1593-1612.
[9]
Goldenberg RL, Culhane JF, Iams JD, et al. Epidemiology and causes of preterm birth[J]. Lancet, 2008, 371(9606):75-84.
[10]
Weissenbacher T, Laubender RP, Witkin SS, et al. Diagnostic biomarkers of pro-inflammatory immune-mediated preterm birth[J]. Arch Gynecol Obstet, 2013, 287(4):673-685.
[11]
Chan RL. Biochemical markers of spontaneous preterm birth in asymptomatic women[J]. Biomed Res Int, 2014, 2014:164081.
[12]
El-Shazly S, Makhseed M, Azizieh F, et al. Increased expression of pro-inflammatory cytokines in placentas of women undergoing spontaneous preterm delivery or premature rupture of membranes[J]. Am J Reprod Immunol, 2004, 52(1):45-52.
[13]
Lim JK, Lisco A, McDermott DH, et al. Genetic variation in OAS1 is a risk factor for initial infection with West Nile virus in man[J]. PLoS Pathog, 2009, 5(2):e1000321.
[14]
Qu HQ, Polychronakos C. Reassessment of the type I diabetes association of the OAS1 locus[J]. Genes Immun, 2009, 10 (Suppl 1):S69-S73.
[15]
Barkhash AV, Perelygin AA, Babenko VN, et al. Variability in the 2'-5'-oligoadenylate synthetase gene cluster is associated with human predisposition to tick-borne encephalitis virusinduced disease[J]. J Infect Dis, 2010, 202(12):1813-1818.
