Mahmud Salaheddin M, Robinson Keira, Richardson Harriet, Tellier Pierre-Paul, Ferenczy Alex S, Roger Michel, Coutlee Francois, Franco Eduardo L
Division of Cancer Epidemiology, McGill University, Montreal, Quebec, Canada.
J Infect Dis. 2007 Jul 1;196(1):82-90. doi: 10.1086/518612. Epub 2007 May 29.
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.
A cohort study of cervical HPV infections was used to examine the role that 5 HLA alleles (B07, DQB103, DQB10602, DRB113, 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.
HLA DRB113 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]). DQB103 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.
The results of this study support the hypothesis that certain HLA class II polymorphisms mediate genetic susceptibility to the acquisition of HPV infection.
只有少数人乳头瘤病毒（HPV）感染的女性最终会发展为宫颈癌，这表明宿主免疫机制在该疾病中发挥作用。HLA多态性与宫颈癌风险相关，但对于它们在HPV感染的获得和持续存在中所起的作用知之甚少。
采用一项关于宫颈HPV感染的队列研究，以检验5种HLA等位基因（B07、DQB103、DQB10602、DRB113和DRB1*1501）在确定蒙特利尔524名女大学生HPV阳性和持续感染风险中所起的作用。通过使用MY09/11聚合酶链反应方案确定HPV阳性。使用序列特异性引物的聚合酶链反应技术对宫颈标本纯化DNA中的HLA等位基因进行分型。
HLA DRB113与HPV感染的累积风险相关（优势比[OR]，1.7[95%置信区间{CI}，1.0 - 2.8]），与致癌性HPV相关（OR，1.6[95%CI，0.9 - 2.8]），与HPV - 16相关（OR，2.0[95%CI，0.9 - 4.4]）。DQB103始终与较低的HPV感染累积风险相关，但这种关联无统计学意义。没有一个等位基因影响HPV持续感染的风险。
本研究结果支持以下假设，即某些HLA II类多态性介导对HPV感染获得的遗传易感性。
