OBJECTIVE: To evaluate clustering patterns of prevalent infection with multiple human papillomavirus (HPV) types in 8365 nonhysterectomized women from the Guanacaste Study of HPV Natural History. METHODS: HPV testing was performed on cervical cells by MY09/M11 L1 degenerate consensus primer polymerase chain reaction method, with dot-blot hybridization for genotyping. Logistic regression was used to model type-specific HPV positivity, adjusted for age, lifetime number of sexual partners, and specific HPV type prevalence. Woman-level random effects were added to represent unobservable risk factors common to all HPV types. RESULTS: The observed-to-expected ratio for infections with 2 types was 1.16 (95% credible interval: 1.11-1.21) and for ≥3 types was 1.04 (95% credible interval: .96-1.13). The tendency of HPV types to cluster increased significantly with the genetic similarity of L1 regions. P value < .01 was observed for 2 HPV pairs: HPV-62 and -81 were found together more, while HPV-51 and -71 were found together less often than expected. CONCLUSIONS: We found a small degree of aggregation between any HPV types and lack of clustering between specific carcinogenic types. Our data indirectly provide reassurance on lack of misclassification for the large majority of HPV types in multiple infections detected by the MY09/11 method and genotyped using dot-blot hybridization.
OBJECTIVE: To evaluate clustering patterns of prevalent infection with multiple human papillomavirus (HPV) types in 8365 nonhysterectomized women from the Guanacaste Study of HPV Natural History. METHODS:HPV testing was performed on cervical cells by MY09/M11 L1 degenerate consensus primer polymerase chain reaction method, with dot-blot hybridization for genotyping. Logistic regression was used to model type-specific HPV positivity, adjusted for age, lifetime number of sexual partners, and specific HPV type prevalence. Woman-level random effects were added to represent unobservable risk factors common to all HPV types. RESULTS: The observed-to-expected ratio for infections with 2 types was 1.16 (95% credible interval: 1.11-1.21) and for ≥3 types was 1.04 (95% credible interval: .96-1.13). The tendency of HPV types to cluster increased significantly with the genetic similarity of L1 regions. P value < .01 was observed for 2 HPV pairs: HPV-62 and -81 were found together more, while HPV-51 and -71 were found together less often than expected. CONCLUSIONS: We found a small degree of aggregation between any HPV types and lack of clustering between specific carcinogenic types. Our data indirectly provide reassurance on lack of misclassification for the large majority of HPV types in multiple infections detected by the MY09/11 method and genotyped using dot-blot hybridization.
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