HLA Polymorphisms and Cervical Human Papillomavirus Infection in a Cohort of Montreal University Students

• Published in: The Journal of infectious diseases Vol. 196; no. 1; pp. 82 - 90
• Main Authors: Mahmud, Salaheddin M., Robinson, Keira, Richardson, Harriet, Tellier, Pierre-Paul, Ferenczy, Alex S., Roger, Michel, Coutlée, François, Franco, Eduardo L.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01-07-2007; University of Chicago Press
• Subjects: Adolescent; Adult; Alleles; Biological and medical sciences; Canada; Cervical cancer; Cervix Uteri - virology; Cohort Studies; Coitus; Ethnicity; Female; Fundamental and applied biological sciences. Psychology; Gene Frequency; Genetic Predisposition to Disease; Genotype; Haplotypes; HLA antigens; HLA Antigens - genetics; Human papillomavirus; Human papillomavirus 16; Humans; Immunity, Innate - genetics; Infections; Infectious diseases; Medical sciences; Microbiology; Middle Aged; Miscellaneous; Neoplasia; Papillomaviridae - physiology; Papillomavirus Infections - epidemiology; Papillomavirus Infections - genetics; Polymerase Chain Reaction - methods; Polymorphism, Genetic; Risk Factors; Statistical significance; Students; Universities; Virology; Viruses; Canada; Papillomavirus; Virus; Infection; HLA-System; Human papillomavirus; Microbiology; Papovaviridae; Student; Polymorphism
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/518612

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 polymerasechain-reaction protocol. HLA alleles from purified DNA from cervical specimens were typed by use of a polymerasechain-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.