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Long-term Impact of Human Papillomavirus Vaccination on Infection Rates, Cervical Abnormalities, and Cancer Incidence

Bogaards, Johannes A.a,b; Coupé, Veerle M. H.a; Xiridou, Mariab; Meijer, Chris J. L. M.c; Wallinga, Jaccob,d; Berkhof, Johannesa

Erratum

Reference

Bogaards JA, Coupe VMH, Xiridou M, et al. Long-term impact of human papillomavirus vaccination on infection rates, cervical abnormalities, and cancer incidence. Epidemiology. 2011;22;505–515.

In the Appendix of the paper “Long-term Impact of Human Papillomavirus Vaccination on Infection Rates, Cervical Abnormalities, and Cancer Incidence,” the formula for the lifetime risk of infection was given by (page 7 of the eAppendix, http://links.lww.com/EDE/A484):

This formula makes no correction for the probability of remaining virgin up to age a, and is valid only for those who initiate sexual activity at the model starting age of 10 years. The lifetime infection risk will be much lower for the average woman, and should be calculated as:

Consequently, the numbers reported in the Abstract should read:

At 50% vaccine coverage, the estimated lifetime infection risk in nonvaccinated women dropped from 0.46 (95% credible interval = 0.35–0.54) to 0.37 (0.26–0.46) for HPV-16, and from 0.40 (0.32–0.46) to 0.31 (0.22–0.36) for HPV-18.

The second paragraph of the Results section should start with:

A woman's mean lifetime probability of infection in the prevaccine era is estimated to be 0.46 for type 16 and 0.40 for type 18.

The final sentences of this paragraph should read:

At 50% vaccine coverage, the probability of ever becoming infected with HPV-16 for nonvaccinated women drops from a median of 0.47 (95% CI = 0.35–0.54) to 0.38 (0.26–0.46). For HPV-18, the decline is from a median of 0.41 (0.32–0.46) to 0.31 (0.22–0.36). At 90% vaccine coverage, the lifetime infection risk in nonvaccinated women ultimately drops to 0.10 for HPV-16 (0.02–0.16) and to 0.05 for HPV-18 (0.001–0.10).

Epidemiology. 22(6):881, November 2011.

Epidemiology:
doi: 10.1097/EDE.0b013e31821d107b
Infectious Disease: Original Article
Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Author Information

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).

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com).

Correspondence: Johannes A. Bogaards, Department of Epidemiology and Biostatistics, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail: j.bogaards@vumc.nl.

© 2011 Lippincott Williams & Wilkins, Inc.