Encouraging reductions in the incidence of genital warts have been reported in Australia since the commencement of the National Human Papillomavirus (HPV) Vaccination Program1 in 2007. Every year, the Program, which is a part of the National Immunisation Program (NIP), provides a free school-based vaccination for 12- to 13-year-old girls. A catch-up vaccination campaign for 13- to 26-year-old females was conducted as a part of the Program and ceased in 2009.
The vaccine delivered under the Program is the quadrivalent vaccine Gardasil manufactured by Merck.2 The coverage achieved to date by vaccination in the targeted population is around 80% (for 2 doses).3
Recently published data collected at a large urban sexual health clinic in Australia show a dramatic decline in the proportion of new clients with genital warts in both young women and men as of June 2011.4 Similar results were reported for national sentinel surveillance data obtained from 8 large Australian sexual health clinics.5,6 Although the extent to which these declines reflect what is happening in the general Australian population is unknown, it is expected that genital wart incidence will also have dropped substantially at the population level. In 2013, vaccination for boys aged 12 years also commenced under the NIP (14- to 15-year-old boys are covered by a 2-year catch-up vaccination, which started in 2013), and this is expected to result in even greater reductions in genital warts.
We developed a mathematical transmission model for HPV types 6 and 11, which, together, are responsible for more than 90% of genital warts.7 Our aim was to estimate temporal changes in relative reductions in genital warts in the Australian heterosexual population after the introduction of male vaccination and also to test consistency of the model output with the reported reductions to date.
A mathematical dynamic model of HPV-6/11 transmission in the Australian heterosexual population was developed to predict temporal changes in genital wart incidence as a result of vaccination. We treated HPV-6 and HPV-11 as a single combined HPV type 6/11. Although a complete description of the model, including structure, key assumptions, and parameter values, is provided in the Technical Appendix (Supplemental Digital Content 1, http://links.lww.com/OLQ/A78), it is pertinent to note here that the model was compartmental and deterministic, with the population viewed as a number of nonoverlapping groups. The groups (compartments), defined based on HPV infection status, are illustrated schematically in Figure 1. We simulated movement between the compartments as depicted in Figure 1 by means of arrows. The model was fitted to age-specific prevaccination Australian genital wart incidence data,8 and the simulated incidence was compared with that reported9 for a number of years after the commencement of vaccination.
Human papillomavirus vaccination in our model is implemented in a manner designed to mirror the coverage achieved to date in the NIP1,3,10 and the extension of the program to include males from 2013. We assume a vaccine coverage of 80% for ongoing female vaccination, as has been achieved for 2 doses. The school-based male vaccination for 12- to 13-year-old boys began in 2013, and a catch-up campaign to cover boys aged 14 to 15 years is also underway and will last for 2 years. As for girls, we assume a vaccine coverage of 80% for ongoing male vaccination and for the catch-up program for 2 years.
We assume the vaccine efficacy against transmission to be 100% for females and 90% for males based on the mean efficacies against genital warts for HPV-6/11/16/18 for the per-protocol population from the Gardasil clinical trials.11,12
Vaccination Program to Date (2007–2011)
Model-predicted and reported6,9 short-term relative reductions in genital wart incidence in selected female and male cohorts are shown in Figure 2. Note the sharp drop in reported relative reductions in females by the end of 2008. By 2009, reductions predicted by the model were more consistent with these observed reductions. In males, the reductions, presumed to be attributable to herd immunity, were notable by the end of 2008 and even more pronounced by the end of 2009. This is not surprising given that a substantial proportion of the female cohort we consider was vaccinated during the catch-up campaign of 2007 to 2009 and can be presumed to have been already sexually active.
Extended Vaccination Program (From 2013)
Predicted relative reductions in genital wart incidence, for heterosexual males and females in Australia, under both the current and an extended vaccination program, which includes male vaccination from 2013, are shown in Figure 3. After 6 years of vaccination, the model predicts relative reductions of approximately 70% and 65% in females and males, respectively. The effect of male vaccination, although marginal for several years after 2013, will already be substantial by 2020 and will increase steadily until 2030. In particular, the relative reductions in the incidence of genital warts in females will be around 80% by 2021, which is an additional 7% reduction compared to the female-only vaccination. Similarly, in males the reductions will reach 75% (12% greater than for female-only vaccination).
Based on the predictions of our model, we expect that by 2030, the relative reductions in females will exceed 90% (and approach 90% in males) with male vaccination, whereas without male vaccination, these reductions would be less than 80% (females) and close to 65% (males). At the postvaccination equilibrium (when HPV infection level in the population no longer changes), predicted to be reached around 2060, male vaccination will provide an additional 9% in relative reductions in females and 23% in males in comparison with female-only vaccination.
Predictions from our model are consistent with sentinel surveillance data suggesting that the incidence of genital warts in Australia is declining. The estimations with female-only vaccination, however, show that the decline in the cohorts we selected for analysis should begin to slow down in 2010 to 2011, whereas the reported data suggest a pronounced deceleration of the decline from 2009 (males) and 2010 (females). This trend is cohort specific and relevant only in the context of the 2007 to 2009 catch-up vaccination. Indeed, the effect of the yearly school-based vaccination in the considered cohorts is represented via the girls aged 12 in 2007 (ie, 16 in 2011), who are likely to only have started to become sexually active from around 2011.
It is predicted that the introduction of male vaccination will be accompanied by substantially increased reductions in genital wart incidence in the heterosexual Australian population compared with the current female-only vaccination. In particular, model predictions are that vaccination of males and females will result in near elimination of genital warts in the population, whereas under the female-only program, we would expect to observe up to 85% reduction in genital wart incidence in females and around 75% in heterosexual males (Fig. 2).
However, it should be noted that complete elimination of genital warts is unlikely to happen in reality. Our model does not account for the contribution to genital warts in Australia because of immigration and travel. The model also does not include men who have sex with men who benefit little from the current female-only vaccination program.2 The extension of the NIP to include male vaccination will clearly result in benefits for men who have sex with men, which will be evaluated by future studies.
Australia was the first country to implement a publicly funded HPV vaccination program and the first to approve male vaccination. The findings from our study suggest that these world-leading programs will achieve near elimination of genital warts in Australia.
1. Australian Government. Department of Health and Ageing. Information About the National Human Papillomavirus (HPV) Vaccination Program. Accessed September 13, 2012.
2. Gardasil Web site. Available at: www.gardasil.com
. Accessed September 13, 2012.
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