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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. [ABSTRACT FROM AUTHOR]

Abstract: Background: The association between human papillomavirus (HPV) viral load and high-grade squamous intraepithelial lesion (HSIL) of the uterine cervix has been demonstrated for high-risk HPV-16 but has not been investigated for low-risk HPV types. Objective: To determine the association between the presence of low-grade SIL (LSIL) and viral load of low-risk HPV type 6. Study design: 107 HPV-6-positive cytobrush samples collected from 90 women (67 without SIL, 11 with LSIL, 5 with HSIL, 6 with SIL of unknown grade and 1 with a smear with LSIL and a normal colposcopy) were analyzed for their content of HPV-6 DNA. Methods: HPV-6 E6 and E2 DNA loads were measured in the cytobrush samples with two real-time PCR assays. HPV-6 integration was confirmed with restriction-site PCR. Results: HPV-6 DNA in cervical samples ranged from 1.8×102 to 4.25×108 copies per μg of cellular DNA. HPV-6 E6 DNA loads were higher in women with LSIL, with or without co-infection with high-risk HPV types, than in women without SIL (p =0.03). HPV-6 loads greater than 8.76×106 copies per μgDNA, corresponding to the mean HPV-6 load measured in women with LSIL, were more frequently detected in these women with LSIL than in women without LSIL, controlling for age (odds ratio 13.5, 95% confidence interval 1.1–172.4). Although 10 samples generated HPV-6 E6/E2 ratios above 2, there was no evidence of integration of HPV-6 by restriction-site PCR. Conclusion: Samples from women with LSIL contained higher HPV-6 loads than women without SIL. HPV-6 DNA was not integrated into cellular DNA in these samples. [Copyright &y& Elsevier]