Papillomavirus and vulvovaginal neoplasia.

Cumulative evidence strongly implicates human papillomavirus (HPV) in the genesis of squamous neoplasia of the lower female genital tract, including the vulva. The association of HPV with neoplasms at that site includes the relationship of specific HPV types with neoplasms and evidence that those HPV DNA types can transform epithelial cells in vitro. The capacity for in vitro transformation has been isolated to specific regions of the HPV genome. That may be unique in cancer-associated viruses. Nevertheless, epidemiologic evidence points to additional factors, including immunologic, habitual and environmental, that may play an important role in the development of lower genital tract carcinomas. In particular, the marked differences in mean age and other variables between women with vulvar precancers and invasive cancer suggest that the evolution of invasive cancer involves more than HPV infection alone. Hence, the prevention of invasive vulvar cancer in older age groups will require an understanding of the unique host factors that render a small group of women susceptible to the disease in the face of an epidemic of HPV infection in the population at large.