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. 2018 Apr;45(4):260-265.
doi: 10.1097/OLQ.0000000000000731.

Non-Vaccine-Type Human Papillomavirus Prevalence After Vaccine Introduction: No Evidence for Type Replacement but Evidence for Cross-Protection

Non-Vaccine-Type Human Papillomavirus Prevalence After Vaccine Introduction: No Evidence for Type Replacement but Evidence for Cross-Protection

Mónica Saccucci et al. Sex Transm Dis. 2018 Apr.

Abstract

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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Conflict of interest statement

Conflict of Interest and Sources of Funding

Dr Kahn has co-chaired 2 National Institutes of Health–funded human papillomavirus (HPV) vaccine clinical trials in HIV-infected individuals, for which Merck & Co, Inc, provided vaccine and immunogenicity titers. Dr Franco has served as occasional advisor to companies involved with HPV vaccination (Merck, GSK) and HPV and cervical cancer diagnostics (Roche, BD, Qiagen). His institution has received unconditional funding from Merck for investigator-initiated studies carried out in his unit. Dr Brown has received honoraria and grant support from Merck, and his institution Indiana University and Merck have a confidential agreement that pays the university based on certain landmarks of vaccine development; Dr Brown receives a portion of this money as income. For the remaining authors, no competing financial interests exist.

Figures

Figure 1.
Figure 1.
Proportions and 95% confidence intervals of vaccinated and unvaccinated women with non–vaccine-type HPV, as well as proportions of vaccinated and unvaccinated women with types genetically related to HPV-16 (A9 species) and HPV-18 (A7 species), adjusted for propensity scores, across the 3 study waves (2006–2014).

References

    1. Jemal A, Simard EP, Dorell C, et al. Annual report to the Nation on the Status of Cancer, 1975–2009, featuring the burden and trends in human papillomavirus (HPV)–associated cancers and HPV vaccination coverage levels. J Natl Cancer Inst 2013; 105:175–201. - PMC - PubMed
    1. Forman D, de Martel C, Lacey CJ, et al. Global burden of human papillomavirus and related diseases. Vaccine 2012; 30(Suppl 5):F12–F23. - PubMed
    1. Joura EA, Leodolter S, Hernandez-Avila M, et al. Efficacy of a quadrivalent prophylactic human papillomavirus (types 6, 11, 16, and 18) L1 virus–like-particle vaccine against high-grade vulval and vaginal lesions: A combined analysis of three randomised clinical trials. Lancet 2007; 369:1693–1702. - PubMed
    1. Lehtinen M, Paavonen J, Wheeler CM, et al. Overall efficacy of HPV-16/18 AS04-adjuvanted vaccine against grade 3 or greater cervical intraepithelial neoplasia: 4-Year end-of-study analysis of the randomised, double-blind PATRICIA trial. Lancet Oncol 2012; 13:89–99. - PubMed
    1. Villa LL, Costa RL, Petta CA, et al. High sustained efficacy of a prophylactic quadrivalent human papillomavirus types 6/11/16/18 L1 virus–like particle vaccine through 5 years of follow-up. Br J Cancer 2006; 95:1459–1466. - PMC - PubMed

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