Updating the natural history of hpv and anogenital cancer Hot sex girls free chat on skype
Individual women enter the model at age 9 years with a healthy cervix and face monthly probabilities of acquiring HPV (HPV16, 18, 31, 33, 45, 52, and 58, other grouped high-risk types, and grouped low-risk types) and transitioning between HPV-related health states (e.g., normal, HPV infection, cervical intraepithelial neoplasia, grades 2 (CIN2) and 3 (CIN3) and cervical cancer) until death, either from background causes or cervical cancer after its onset.
Transitions may be a function of duration (i.e., time since HPV infection or precancer development), HPV genotype, age, and history of HPV infections.
We used the model to simulate a cohort of women in the absence of screening or HPV vaccination to project the cumulative number of causal HPV infections by age and HPV genotype (i.e., HPV16- vs. For each cancer case observed in the model, we identified the age at which the individual women acquired their HPV infection that developed into a clinically detected cancer (i.e., cancers that remained undetected throughout a woman’s lifetime were excluded) (Figure 1).
To isolate the direct benefits of extending the vaccine target age on age-specific cancer incidence, we simulated seven scenarios in which the age of HPV vaccination was varied (i.e., ages 9, 12, 18, 25, 30, 35, or 45 years) in the absence of cervical cancer screening.
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.
To enumerate the direct benefits (excluding herd immunity) of extending the target age of HPV vaccination, we evaluated the health benefits associated with later vaccination age on age-specific cervical cancer incidence rates.
Our model projected that among all cervical cancers, 50% and 75% of women acquired their causal HPV infection by ages 20.6 (range: 20.1–21.1) and 30.6 (range: 29.6–31.6) years, respectively. Assuming 95% efficacy against HPV16 and HPV18 infections, the direct reduction in lifetime risk of cervical cancer varied from 55% (53–56%) among women vaccinated at age 9 years to 6% (range: 6–7%) among women vaccinated at age 45 years.
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].The risk of acquiring cervical human papillomavirus (HPV) infections, causally linked to several cancers and genital warts, peaks shortly after sexual initiation, subsequently declining with age in most women .Following acquisition, high-risk HPV infections may persist and progress to a precancerous lesion, a proportion of which will become invasive cancer over time  if not detected and treated in a timely fashion.In settings without existing screening programs, the impact of HPV vaccination at older ages on long-term outcomes will inform whether secondary prevention approaches, such as HPV testing, should also be coupled with an HPV vaccination policy.
The optimal choice of intervention(s) will be determined by the cumulative proportion of causal infections that have already been acquired at the time of vaccination, and thereby the resulting cancer could only be prevented through screening, diagnosis, and treatment of the antecedent cervical precancer, compared with those that are yet to be acquired and could be prevented via HPV vaccination .
In the absence of primary (i.e., HPV vaccination) or secondary (i.e., screening) prevention, our model projected that among all cervical cancers, 50% and 75% of women acquired their causal HPV infection by ages 20.6 (20.1–21.1) and 30.6 (29.6–31.6) years, respectively (Figure 2, left panel).