Human papillomavirus (HPV) vaccines: prospects for eradicating cervical cancer.

Journal of Family Planning and Reproductive Health Care 2004: 30(4) Introduction One of the most important developments of the past 25 years in cancer biology has been the evidence that infection with human papillomaviruses (HPVs) in the lower genital tract is the cause of virtually all cases of cervical carcinoma in women and a smaller, less defined fraction of vulvar, vaginal, anal and penile cancers. HPVs are members of a large family of viruses that infect squamous epithelial surfaces: the 35 HPV types that infect the genital tract fall into two discrete groups: ● Low-risk, non-oncogenic types 6 and 11 and their relatives that cause anogenital warts and are rarely detected in malignant disease. ● High-risk, oncogenic HPVs (hrHPV) types 16, 18, 31, 33, 35, 45, 52, 56 plus about eight other minor types. These can be detected in almost 100% of cervical cancer biopsies and more than 90% of the high-grade, cervical intra-epithelial neoplasia (CIN2/3) precursor lesions. The causal link between HPV infection and cervical cancer has now been established beyond reasonable doubt.1 HPV 16 is the most frequently detected HPV in cervical cancers (about 50–60%) with HPV 18 (10–12%) being the second most common. The implication of this is that intervention against this viral infection should prevent the vast majority of cervical cancer cases worldwide. Vaccines are the traditional costeffective means to prevent microbialand viral-induced diseases: HPV should be no exception and, indeed, substantial progress has been made in the past decade in the development of vaccines to prevent and/or treat these infections. Prophylactic HPV vaccines are in large Phase III trials, and several Phase II trials of therapeutic vaccines for the treatment of established HPV-induced intraepithelial disease are either complete or in progress.