title: Genetic susceptibility to norovirus GII.3 and GII.4 infections in Chinese pediatric diarrheal disease.
abstract: BACKGROUND
  Noroviruses (NoVs) are a leading cause of viral diarrhea in young children. Secretor status has been confirmed to be linked with Norwalk virus (NoV GI.1) infection but there is limited information about whether secretor genotypes are associated with pediatric NoV epidemic strains in vivo.
  
  
  METHODS
  In this study, fecal specimens and serum samples were collected from 124 hospitalized children with acute diarrhea in Xi'an, China. TaqMan real-time reverse transcription polymerase chain reaction was used to detect NoVs in fecal samples, and NoV-positive samples were further verified using conventional reverse transcription polymerase chain reaction and sequenced. DNA was extracted from sera and TaqMan single-nucleotide polymorphism genotyping assay was applied to determine the FUT2 A385T polymorphism.
  
  
  RESULTS
  Only NoV GII.3 and GII.4 genotypes were found in NoV-positive samples, and NoVs were detected in 25% (15/60), 40.5% (17/42) and 9.1% (2/22) of children with homozygous secretor genotype (Se 385 Se 385), heterozygous secretor genotype (Se 385 se 385) and homozygous weak secretor genotype (se 385 se 385), respectively. Children with secretor genotypes Se 385 Se 385 and Se 385 se 385 were significantly (P < 0.05) more susceptible to combined NoV GII.3 and GII.4 infections than children with weak secretor genotype se 385 se 385.
  
  
  CONCLUSIONS
  These findings indicate that secretor positivity is significantly associated with GII.3 and GII.4 infections in Chinese pediatric diarrheal disease and the weak secretor phenotype does not completely protect children from GII.3 and GII.4 infections.
authors.affiliation: From the *Rollins School of Public Health, Emory University, Atlanta, GA; †School of Public Health, Xi'an Jiaotong University, Xi'an, China; ‡National Institute of Public Health and the Environment, Bilthoven, The Netherlands; and §Boston University Medical Center, Boston, MA.
authors.forename: Pengbo
authors.initials: P
authors.lastname: Liu
authors.forename: Xiaoqin
authors.initials: X
authors.lastname: Wang
authors.forename: Joong-Chul
authors.initials: JC
authors.lastname: Lee
authors.forename: Peter
authors.initials: P
authors.lastname: Teunis
authors.forename: Senke
authors.initials: S
authors.lastname: Hu
authors.forename: Helen Tang
authors.initials: HT
authors.lastname: Paradise
authors.forename: Christine
authors.initials: C
authors.lastname: Moe
mesh_terms: D000914:Antibodies, Viral / Q000097:blood*; D044466:Asian People / Q000235:genetics; D017250:Caliciviridae Infections / Q000235:genetics* / Q000382:microbiology; D002675:Child, Preschool; D002681:China; D003967:Diarrhea / Q000382:microbiology*; D005243:Feces / Q000821:virology; D005647:Fucosyltransferases / Q000235:genetics*; D005759:Gastroenteritis / Q000382:microbiology*; D020022:Genetic Predisposition to Disease; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007223:Infant; D020125:Mutation, Missense; D029322:Norovirus / Q000276:immunology*; D020641:Polymorphism, Single Nucleotide; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D000914:Antibodies, Viral; D005647:Fucosyltransferases; D007074:Immunoglobulin G; D000097631:Galactoside 2-alpha-L-fucosyltransferase