Model for assessing human papillomavirus vaccination strategies

Abstract

We present a transmission dynamic model that can assess the epidemiologic consequences and cost-effectiveness of alternative strategies of administering a prophylactic quadrivalent (types 6/11/16/18) human papillomavirus (HPV) vaccine in a setting of organized cervical cancer screening in the United States. Compared with current practice, vaccinating girls before the age of 12 years would reduce the incidence of genital warts (83%) and cervical cancer (78%) due to HPV 6/11/16/18. The incremental cost-effectiveness ratio (ICER) of augmenting this strategy with a temporary catch-up program for 12- to 24-year-olds was US $4,666 per quality-adjusted life year (QALY) gained. Relative to other commonly accepted healthcare programs, vaccinating girls and women appears cost-effective. Including men and boys in the program was the most effective strategy, reducing the incidence of genital warts, cervical intraepithelial neoplasia, and cervical cancer by 97%, 91%, and 91%, respectively. The ICER of this strategy was $45,056 per QALY.

Figure 1

A simplified schematic diagram of human papillomavirus (HPV) infection and disease state transitions, lifetime duration of infection-derived immunity, unvaccinated compartments. A) Persons enter into the susceptible (X) compartment and leave all compartments at sex- and age-specific rate. A susceptible host may be infected by either or both HPV types. A host infected with a given type can also be infected with the other type and move into compartment (Y¹²). An infected person can clear infection with 1 type and can become immune to that type (Z^h) and get infected with the other type (U^h). Infection with and clearance of all types results in lifetime immunity. B) Cervical intraepithelial neoplasia (CIN) develops in females and progresses though several histologic states: infected with a normal cervix; CIN 1; CIN 2; CIN 3; localized, regional, and distant cervical cancer. CIN can regress to normal with or without infection. Genital warts can develop and clear in those infected with HPV 6/11.

Figure 2

Human papillomavirus (HPV) prevalence by sex and age group, as predicted by the model and reported in selected studies from North America. HPV high risk includes types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82.

Figure 3

Incidence of cervical intraepithelial neoplasia (CIN) 2/3 due to human papillomavirus 6/11/16/18 infection among girls and women >12 years of age, by vaccination strategy.

Figure 4

Incidence of cervical cancer due to human papillomavirus 16/18 infection among girls and women >12 years of age, by vaccination strategy.

Figure 5

A) Incidence of genital warts due to human papillomavirus (HPV) 6/11 infection among boys and men >12 years of age by strategy. B) Incidence of genital warts due to HPV 6/11 infection among girls and women >12 years, of age by strategy.

Figure 6

Sensitivity analysis. A) Incidence of genital warts due to human papillomavirus (HPV) 6/11 infection among boys and men >12 years of age, by strategy, 10 years’ duration of protection. B) Incidence of genital warts due to (HPV 6/11 infection among girls and women >12 years of age by strategy, 10 years’ duration of protection.

Figure 7

Sensitivity analysis. A) Incidence of cervical cancer due to human papillomavirus (HPV) 16/18 infection among girls and women >12 years of age with 50% coverage. B) Incidence of cervical cancer due to HPV 16/18 infection among girls and women >12 years of age with 90% coverage.

Figure 8

Impact of age that vaccination was begun on cervical cancer incidence due to human papillomavirus 16/18 infection among girls and women >12 years of age.