title: Association between HLA-DRB1 polymorphism, high-risk HPV infection and cervical neoplasia in southern Chinese.
abstract: Multiple determinants are involved in the progression of human papillomavirus (HPV)-infected cervical lesion to invasive cancer. Human leukocyte antigen (HLA) polymorphism seems to play a role. This study examined the association between HLA-DRB1 polymorphism, high-risk HPV infection, and the development of cervical neoplasia in southern Chinese. Three hundred and seventy women with cervical neoplasia (43 cervical intraepithelial neoplasia grade II, 154 grade III, and 173 invasive cancers) and 323 controls were recruited for HLA-DRB1 typing by a sequence-based approach. Cervical specimens were collected for HPV detection by a consensus primer-based polymerase chain reaction, and with the type of HPV identified by hybridization with type-specific oligonucleotide probes. A protective effect of HLA-DRB1*12 for cervical neoplasia was observed, and with stronger associations when subgroup analyses were carried out for patients infected with HPV16 and HPV58. The protective effect of HLA-DRB1*13 that had been reported from other populations was not observed. The data obtained in this study showed that HLA-DRB1*03 conferred a higher risk for HPV18-infected, but not for HPV16-, HPV52-, or HPV58-infected cervical lesions. Although, HPV52 was reported as uncommon worldwide, it was found to be the second most prevalent type in the southern Chinese population. However, no additional risk association was observed when subgroup analyses were performed for HPV52-infected patients. The current study shows that, among southern Chinese, the outcome of HPV-infected cervical lesions is associated with HLA-DRB1 polymorphism. These associations often vary with the type of HPV infection.
authors.affiliation: Department of Microbiology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong Special Administrative Region, Hong Kong, China. paulkschan@cuhk.edu.hk
authors.forename: Paul K S
authors.initials: PK
authors.lastname: Chan
authors.forename: Tak-Hong
authors.initials: TH
authors.lastname: Cheung
authors.forename: C K
authors.initials: CK
authors.lastname: Lin
authors.forename: Shing-Shun N
authors.initials: SS
authors.lastname: Siu
authors.forename: So-Fan
authors.initials: SF
authors.lastname: Yim
authors.forename: Keith W K
authors.initials: KW
authors.lastname: Lo
authors.forename: Jo L K
authors.initials: JL
authors.lastname: Cheung
authors.forename: Ann O Y
authors.initials: AO
authors.lastname: Tam
authors.forename: Julian W
authors.initials: JW
authors.lastname: Tang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D044466:Asian People / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D006684:HLA-DR Antigens / Q000235:genetics*; D059811:HLA-DRB1 Chains; D006723:Hong Kong; D052162:Human papillomavirus 16 / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D027383:Papillomaviridae / Q000145:classification / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity; D030361:Papillomavirus Infections / Q000235:genetics* / Q000276:immunology* / Q000821:virology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000276:immunology* / Q000821:virology; D002578:Uterine Cervical Dysplasia / Q000235:genetics / Q000276:immunology / Q000821:virology
chemical_list: D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains