Dynamic, compartmental, HPV 16 model
Model overview. The UW model is an open-cohort, age-structured, compartmental, deterministic human papillomavirus (HPV) transmission model stratified by HPV-16/18 and other high-risk HPV types. It also includes cervical carcinogenesis, HPV vaccination and cervical cancer screening.
Cervical carcinogenesis. Women and men enter the susceptible pool upon sexual debut, and with each partnership, face a risk of HPV acquisition depending on the number of new partners, the prevalence of HPV in the population (generated “dynamically” each cycle in the model), and the probability of HPV transmission per susceptible-infected partnership. Women transition from the uninfected to the HPV-infected state, to low- (cervical intraepithelial neoplasia [CIN I]) and high-grade (CIN II and III) pre-cancer and cervical cancer. The model allows for hysterectomy (including reasons other than cervical cancer treatment) at any stage and accounts for the impact of smoking on cervical cancer rates. (1) Men transition between the susceptible and the HPV-infected state.
HPV transmission, vaccination and screening. As described previously (2-3), the model captures the transmission of HPV by estimating the force of infection, which is a function of sexual mixing (by age and activity class), the proportion of infected individuals in the population (generated internally in the model each cycle) and the HPV transmission probability. (4) Vaccination and screening decreases the incidence of HPV according to demonstrated clinical efficacy, leading to the decrease in incidence of subsequent disease states. The screening function accounts for sensitivity and specificity of the screening tool, loss-to-follow-up, and treatment success. Screening and treatment returns a proportion of individuals to the HPV-negative susceptible state, but a proportion experience treatment failure and remain in the disease compartment. The model is able to explore synergies between vaccination and screening, such as a decrease in recurrence of CIN after vaccination.
Calibration and validation. The model was calibrated using data on sexual behavior, national data for HPV seropositivity (5), hysterectomy rates, smoking (1), and uptake of screening by age. HPV progression and regression rates converted to transition probabilities (6) were based on a review the literature (7-8). Independent data on age-specific cervical cancer incidence rates over time were used to validate the model.
Tip: Hover your cursor over the dashed attribute links below for more information. View the details of this model in a grid with other cervical models.
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