title: HLA polymorphisms and cervical human Papillomavirus infection in a cohort of Montreal University students.
abstract: BACKGROUND
  Only a minority of women with human papillomavirus (HPV) infection eventually develop cervical cancer, which suggests that host immune mechanisms play a role in the disease. HLA polymorphisms have been linked to the risk of cervical cancer, but very little is known about the role that they play in the acquisition and persistence of HPV infection.
  
  
  METHODS
  A cohort study of cervical HPV infections was used to examine the role that 5 HLA alleles (B*07, DQB1*03, DQB1*0602, DRB1*13, and DRB1*1501) play in determining the risk of HPV positivity and persistence in 524 female university students in Montreal. HPV positivity was determined by use of the MY09/11 polymerase-chain-reaction protocol. HLA alleles from purified DNA from cervical specimens were typed by use of a polymerase-chain-reaction technique using sequence-specific primers.
  
  
  RESULTS
  HLA DRB1*13 was associated with cumulative risk of HPV infections (odds ratio [OR], 1.7 [95% confidence interval {CI}, 1.0-2.8]), for oncogenic HPV (OR, 1.6 [95% CI, 0.9-2.8]), and for HPV-16 (OR, 2.0 [95% CI, 0.9-4.4]). DQB1*03 was consistently associated with a lower cumulative risk of HPV infections, but this association was not statistically significant. None of the alleles affected the risk of HPV persistence.
  
  
  CONCLUSIONS
  The results of this study support the hypothesis that certain HLA class II polymorphisms mediate genetic susceptibility to the acquisition of HPV infection.
authors.affiliation: Division of Cancer Epidemiology, McGill University, Montreal, Quebec, Canada.
authors.forename: Salaheddin M
authors.initials: SM
authors.lastname: Mahmud
authors.forename: Keira
authors.initials: K
authors.lastname: Robinson
authors.forename: Harriet
authors.initials: H
authors.lastname: Richardson
authors.forename: Pierre-Paul
authors.initials: PP
authors.lastname: Tellier
authors.forename: Alex S
authors.initials: AS
authors.lastname: Ferenczy
authors.forename: Michel
authors.initials: M
authors.lastname: Roger
authors.forename: Francois
authors.initials: F
authors.lastname: Coutlee
authors.forename: Eduardo L
authors.initials: EL
authors.lastname: Franco
mesh_terms: D000293:Adolescent; D000328:Adult; D002170:Canada; D002584:Cervix Uteri / Q000821:virology*; D015331:Cohort Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006680:HLA Antigens / Q000235:genetics*; D006239:Haplotypes; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D008875:Middle Aged; D027383:Papillomaviridae / Q000502:physiology; D030361:Papillomavirus Infections / Q000453:epidemiology* / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013334:Students; D014495:Universities
chemical_list: D006680:HLA Antigens