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.
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: Jian Ming Hu; Qi Sun; Ling Li; Chun Xia Liu; Yun Zhao Chen; Hong Zou; Li Juan Pang; Jin Zhao; Lan Yang; Yu Wen Cao; Xiao Bin Cui; Yan Qi; Wei Hua Liang; Wen Jie Zhang; Feng Li Journal: Int J Clin Exp Pathol Date: 2014-08-15
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Authors: Sofía Bernal-Silva; Julio Granados; Clara Gorodezky; Carmen Aláez; Hilario Flores-Aguilar; Ricardo M Cerda-Flores; Geraldina Guerrero-González; Lezmes D Valdez-Chapa; José Morales-Casas; Juan Francisco González-Guerrero; Hugo A Barrera-Saldaña Journal: Infect Agent Cancer Date: 2013-08-30 Impact factor: 2.965
Authors: Stephanie Metcalfe; Michel Roger; Marie-Claude Faucher; François Coutlée; Eduardo L Franco; Paul Brassard Journal: Int J Circumpolar Health Date: 2013-08-05 Impact factor: 1.228
Authors: Staci L Sudenga; Howard W Wiener; Caroline C King; Anne M Rompalo; Susan Cu-Uvin; Robert S Klein; Keerti V Shah; Jack D Sobel; Denise J Jamieson; Sadeep Shrestha Journal: PLoS One Date: 2014-06-11 Impact factor: 3.240