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Article << Previous     |     Next >>   Contents Vol 4(3)

Modelling the population-level impact of vaccination on the transmission of human papillomavirus type 16 in Australia

David G. Regan A D, David J. Philp B, Jane S. Hocking C, Matthew G. Law A

A National Centre in HIV Epidemiology and Clinical Research, University of New South Wales, Sydney, NSW 2052, Australia.
B The National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT 0200, Australia.
C Key Centre for Women’s Health in Society, School of Population Health, University of Melbourne, Melbourne, Vic. 3010, Australia.
D Corresponding author. Email: d.regan@unsw.edu.au
 
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Abstract

Background: Vaccines are now available to prevent the development of cervical cancer from genital human papillomavirus (HPV) infection. The decision to vaccinate depends on a vaccine’s cost-effectiveness. A rigorous cost-effectiveness model for vaccinated individuals is presented in a companion paper; this paper investigates the additional benefits the community might receive from herd immunity. Methods: A mathematical model was developed to estimate the impact of a prophylactic vaccine on transmission of HPV type 16 in Australia. The model was used to estimate the expected reduction in HPV incidence and prevalence as a result of vaccination, the time required to achieve these reductions, and the coverage required for elimination. The modelled population was stratified according to age, gender, level of sexual activity and HPV infection status using a differential equation formulation. Clinical trials show that the vaccine is highly effective at preventing persistent infection and pre-cancerous lesions. These trials do not, however, provide conclusive evidence that infection is prevented altogether. The possible modes of vaccine action were investigated to see how vaccination might change the conclusions. Results: The model predicts that vaccination of 80% of 12-year-old girls will eventually reduce HPV 16 prevalence by 60–100% in vaccinated and 7–31% in unvaccinated females. If 80% of boys are also vaccinated, reductions will be 74–100% in vaccinated and 86–96% in unvaccinated females. A campaign covering only 12-year-old girls would require 5–7 years to achieve 50% of the eventual reduction. With a catch-up campaign covering 13–26-year-olds, this delay would be reduced to only 2 years. Unrealistically high coverage in both sexes would be required to eliminate HPV 16 from the population. Under pessimistic assumptions about the duration of vaccine-conferred immunity, HPV 16 incidence is predicted to rise in some older age groups. Conclusions: Mass vaccination with a highly effective vaccine against HPV 16 has the potential to substantially reduce the incidence and prevalence of infection. Catch-up vaccination offers the potential to substantially reduce the delay before the benefits of vaccination are observed. A booster vaccination might be required to prevent an increase in incidence of infection in women over 25 years of age.

Keywords: cervical cancer, dynamic transmission model, herd immunity.


   
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