title: Variations in IL-1R1 Gene Influence Risk for Hepatitis B Virus Infection of Children in a Han Chinese population.
abstract: OBJECTIVE
  Host genetic factors play an important role in the pathogenesis of hepatitis B virus (HBV) infection. However, the role of Interleukin1Receptor, Type I (IL-1R1) gene in HBV infection and breakthrough infection in children remains unclear. The aim of this study was to investigate the association between SNPs in IL-1 family and HBV infection and breakthrough infection in children.
  
  
  METHODS
  A total of 627 Chinese children (274 HBV infected children and 353 controls) ages 6 months to 12 years were recruited from October 2013 to May 2015.Six SNPs were genotyped in IL-1R1, Interleukin-1beta (IL-1B) and Interleukin-18 (IL-18) genes.
  
  
  RESULTS
  A statistically significant association was found between genotype AA in rs3917267 (IL-1R1) and HBV infection in children (OR, 1.740; 95%CI, 1.091-2.774; p=0.020), which was also found at allele A (OR, 1.316;95%CI, 1.050-1.648; p=0.017). Furthermore, rs3917267 was also significantly associated with breakthrough infection of HBV in children born of hepatitis B surface antigen (HBsAg) positive mothers (OR,3.675; 95%CI, 1.160-11.646; P=0.027).
  
  
  CONCLUSIONS
  Our study confirmed that genetic variant in IL-1R1(rs3917267) has significant association with HBV infection and HBV breakthrough infection in children, which provides new clues for the study of pathogenesis of chronic HBV infection in children.
authors.affiliation: Department of Epidemiology, School of Public Health and Management, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Fan
authors.affiliation: Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
authors.forename: Yiling
authors.initials: Y
authors.lastname: Cai
authors.affiliation: Department of Epidemiology, School of Public Health and Management, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Huang
authors.affiliation: Foreign Language College of Chongqing Medical University, Chongqing 400016, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Epidemiology, School of Public Health and Management, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing Medical University, Chongqing 400016, China. Electronic address: 1097123703@qq.com.
authors.forename: Lihong
authors.initials: L
authors.lastname: Mu
authors.affiliation: Department of Epidemiology, School of Public Health and Management, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing Medical University, Chongqing 400016, China. Electronic address: zhouli_tj@163.com.
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
mesh_terms: D000483:Alleles; D044466:Asian People / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D002681:China / Q000453:epidemiology; D004196:Disease Outbreaks; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006509:Hepatitis B / Q000453:epidemiology* / Q000235:genetics* / Q000276:immunology; D006510:Hepatitis B Antibodies / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000276:immunology; D006801:Humans; D007223:Infant; D008297:Male; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011159:Population Surveillance; D053573:Receptors, Interleukin-1 Type I / Q000235:genetics*
chemical_list: D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D053573:Receptors, Interleukin-1 Type I
keywords: HBV; breakthrough infection; children; single nucleotide polymorphism