Public Health

Introduction

Human papillomavirus vaccines have potential to reduce cervical cancer incidence and mortality; however, cultural and economic barriers may hinder success in developing countries. We assessed the impact of a single vaccine campaign in Mali with the use of mathematical modeling. Our model shows that decreases in the prevalence of Human papillomavirus infection are proportional to achieved vaccination coverage.

Anogenital human papillomavirus (HPV) infections represent one of the most prevalent sexually transmitted diseases (STDs) worldwide. Mucosal HPV infections are divided into 2 groups according to the risk of malignant progression. Infections with high-risk HPV types (primarily 16, 18, 31, and 45) are strongly associated with the development of cervical cancer, whereas infection with low-risk HPV types (predominantly 6 and 11) causes benign mucosal tumors. Anogenital warts, or condyloma acuminata, are usually benign tumors of the genital mucosa and rank as one of the most prevalent STDs, with an estimated incidence of 1-3 million new cases per year in the United States. The incidence has increased from 2.5- to 4.5-fold during the past 3 decades.

The numerous therapies used to eliminate anogenital warts fall into 2 classes: ablative (physical destructive methods or cytotoxic or antiproliferative compounds) and immune based (predominantly imiquimod and interferon). Although the cure rate is highly variable from study to study, the recurrence rate is generally similar regardless of the therapy used, with an average of 30% of subjects with recurrences within 3 months after therapy. Cell-mediated immune responses appear to play a major role in regression of anogenital warts and are probably down-regulated or modified by HPVs. A characteristic of all HPV lesions is their propensity to spontaneously regress. Spontaneously regressing anogenital warts are massively infiltrated with CD4+ T cells, and an increased level of interleukin-12 expression has been observed. This phenomenon, together with results from animal studies, forms the main argument supporting the rationale for therapeutic vaccination as a potential therapy for HPV-induced diseases (Parkin, 74) (Parkin, 74).

HPV DNA detection

In each investigator's laboratory, various HPV L1 consensus primer polymerase chain reaction (PCR) systems, including MY09/11, PGMY09/11, GP5+/6+, and SPF primers, were used, with detection of products and HPV typing by EIA, reverse line blot, and line probe assay systems. The samples were analyzed in the central laboratory, using a general primer GP5+/GP6+-mediated PCR-EIA method described elsewhere [25]. Briefly, this PCR-EIA method allows the detection of 14 high-risk HPV types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68) and 6 low-risk HPV types (6, 11, 40, 42, 43, and 44), after a general primer GP5+/biotinylated GP6+ (bio GP6+) PCR. For EIA analysis, GP5+/bio GP6+-generated PCR products were captured on streptavidin-coated microwells, denatured by alkaline treatment, hybridized to cocktails of digoxigenin- labeled internal oligonucleotide probes, and detected immunochemically by reading optical density values at different time intervals (1 h, 3 h, and overnight), as described elsewhere [26]. The samples were first assessed for the presence or absence of high-risk and low-risk HPV types, and when HPV was detected, type-specific PCR-EIA was performed (Parkin, 74) ...