BACKGROUND: We examined non-vaccine-type human papillomavirus (HPV) prevalence in a community before and during the first 8 years after vaccine introduction, to assess for (1) type replacement with any non-vaccine-type HPV and (2) cross-protection with non-vaccine types genetically related to vaccine-type HPV. METHODS: Sexually experienced 13- to- 26-year-old women were recruited for 3 cross-sectional studies from 2006 to 2014 (N = 1180). Outcome variables were as follows: (1) prevalence of at least 1 of 32 anogenital non-vaccine-type HPVs and (2) prevalence of at least 1 HPV type genetically related to HPV-16 and HPV-18. We determined changes in proportions of non-vaccine-type HPV prevalence across the study waves using logistic regression with propensity score inverse probability weighting. RESULTS: Vaccine initiation rates increased from 0% to 71.3%. Logistic regression demonstrated that from 2006 to 2014, there was no increase in non-vaccine-type HPV among vaccinated women (adjusted odds ratio [AOR], 1.02; 95% confidence interval [CI], 0.73-1.42), but an increase among unvaccinated women (AOR, 1.88; 95% CI, 1.16-3.04). Conversely, there was a decrease in types genetically related to HPV-16 among vaccinated (AOR, 0.57; 95% CI, 0.38-0.88) but not unvaccinated women (AOR, 1.33; 95% CI, 0.81-2.17). CONCLUSIONS: We did not find evidence of type replacement, but did find evidence of cross-protection against types genetically related to HPV-16. These findings have implications for cost-effectiveness analyses, which may impact vaccine-related policies, and provide information to assess the differential risk for cervical cancer in unvaccinated and vaccinated women, which may influence clinical screening recommendations. The findings also have implications for public health programs, such as health messaging for adolescents, parents, and clinicians about HPV vaccination.
BACKGROUND: We examined non-vaccine-type human papillomavirus (HPV) prevalence in a community before and during the first 8 years after vaccine introduction, to assess for (1) type replacement with any non-vaccine-type HPV and (2) cross-protection with non-vaccine types genetically related to vaccine-type HPV. METHODS: Sexually experienced 13- to- 26-year-old women were recruited for 3 cross-sectional studies from 2006 to 2014 (N = 1180). Outcome variables were as follows: (1) prevalence of at least 1 of 32 anogenital non-vaccine-type HPVs and (2) prevalence of at least 1 HPV type genetically related to HPV-16 and HPV-18. We determined changes in proportions of non-vaccine-type HPV prevalence across the study waves using logistic regression with propensity score inverse probability weighting. RESULTS: Vaccine initiation rates increased from 0% to 71.3%. Logistic regression demonstrated that from 2006 to 2014, there was no increase in non-vaccine-type HPV among vaccinated women (adjusted odds ratio [AOR], 1.02; 95% confidence interval [CI], 0.73-1.42), but an increase among unvaccinated women (AOR, 1.88; 95% CI, 1.16-3.04). Conversely, there was a decrease in types genetically related to HPV-16 among vaccinated (AOR, 0.57; 95% CI, 0.38-0.88) but not unvaccinated women (AOR, 1.33; 95% CI, 0.81-2.17). CONCLUSIONS: We did not find evidence of type replacement, but did find evidence of cross-protection against types genetically related to HPV-16. These findings have implications for cost-effectiveness analyses, which may impact vaccine-related policies, and provide information to assess the differential risk for cervical cancer in unvaccinated and vaccinated women, which may influence clinical screening recommendations. The findings also have implications for public health programs, such as health messaging for adolescents, parents, and clinicians about HPV vaccination.
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