Vaccination against human papillomavirus (HPV) types 16/18 is being implemented in many countries. There may be indirect benefit of HPV vaccination to nonvaccinated women, who may experience a reduced risk of infection with vaccine-preventable types (herd immunity). We attempt to disentangle the direct and indirect effects of HPV vaccination, while accounting for 14 oncogenic HPV types in a dynamic modeling framework.
On the basis of vaccine uptake among preadolescent girls in the Netherlands, we calculated how heterosexual transmission of HPV-16/18 is expected to change as a result of vaccination, and used these predictions in an individual-based simulation model of cervical carcinogenesis that considers 14 high-risk HPV types. Models were parameterized to match prevaccine data on type-specific HPV infection and cervical disease.
At 50% vaccine coverage, the estimated lifetime infection risk in nonvaccinated women dropped from 0.69 (95% credible interval = 0.50–0.85) to 0.49 (0.32–0.68) for HPV-16, and from 0.68 (0.46–0.79) to 0.43 (0.26–0.57) for HPV-18. For the whole population, we calculated an eventual 47% reduction in cervical cancer incidence, with 1 in 4 cases prevented among nonvaccinated women. The number of indirectly averted cancer cases was highest with vaccine coverage between 50% and 70%, approximating 70 cases per 100,000 women born from 2010 onward.
HPV-16/18 vaccination of preadolescent girls will markedly lower infection rates among nonvaccinated women. Reduced transmission of vaccine-preventable HPV becomes a prominent aspect of cervical cancer control, especially in populations with moderate vaccine coverage.
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From the aDepartment of Epidemiology and Biostatistics, VU University Medical Centre, Amsterdam, The Netherlands; bCentre for Infectious Disease Control, National Institute of Public Health and the Environment, Bilthoven, The Netherlands; cDepartment of Pathology, VU University Medical Centre, Amsterdam, The Netherlands; and dJulius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, The Netherlands.
Submitted 11 July 2010; accepted 24 January 2011; posted 3 May 2011.
Supported by the Health Research and Development Council of the Netherlands Organization for Scientific Research (ZonMw grant 50–50110–96–474).
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Correspondence: Johannes A. Bogaards, Department of Epidemiology and Biostatistics, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail: email@example.com.