Updating the natural history of hpv and anogenital cancer
Our objective was to use a well-documented natural history disease simulation model to explicitly identify the age distribution at which individuals acquire their causal HPV infection in the absence of HPV vaccination or screening in order to help guide the optimal use of both.
This model, which is continually updated and refined using emerging empirical data, is well published and has informed cervical cancer prevention policy worldwide [11–16].
However, how these intermediate endpoints translate to prevention of cervical cancer is not known and unlikely to be observed directly through clinical trials.
Furthermore, HPV genotypes targeted by the first-generation vaccines (i.e., HPV16 and HPV18) contribute to a smaller proportion of cancers that develop after age 50 years, resulting in a lower maximum clinical benefit of vaccinating older women [6, 7].
We assumed 95% efficacy against incident vaccine-targeted HPV infections with lifelong durability for both the first-generation bivalent and quadrivalent vaccines that target HPV16 and HPV18 oncogenic genotypes and the second-generation nonavalent vaccine that targets HPV16, 18, 31, 33, 45, 52, and 58 oncogenic genotypes.
In sensitivity analysis, we evaluated the impact of 2 HPV vaccine durability scenarios on the lifetime reductions in cervical cancer incidence.
Search for updating the natural history of hpv and anogenital cancer:
Importantly, the age distribution varied by HPV genotype (Figure 2, right panel) where causal HPV16 infections were generally acquired at a younger age relative to non-HPV16 infections.