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HPV Vaccination for the Prevention of Cervical Intraepithelial Neoplasia
Jessica A. Kahn, M.D., M.P.H.
This Journal feature begins with a case vignette that includes a therapeutic recommendation. A discussion of the clinical problem and the mechanism of benefit of this form of therapy follows. Major clinical studies, the clinical use of this therapy, and potential adverse effects are reviewed. Relevant formal guidelines, if they exist, are presented. The article ends with the author’s clinical recommendations.
A sexually active 18-year-old woman presents to her internist for an annual examination. During the review of her family history, she
Two low-risk types, HPV type 6 (HPV-6) and HPV type 11 (HPV-11), cause more than 90% of anogenital warts and recurrent respiratory papillomatosis.11 Infection with high-risk HPV types causes virtually 100% of cervical cancers, approximately 90% of anal cancers, 50% of vulvar, vaginal, and penile cancers, and 12% of oropharyngeal cancers.12-14 HPV type 16 (HPV-16), HPV type 18 (HPV-18), or both cause approximately 70% of cervical cancers, whereas types 16, 18, 45, 31, 33, 52, 58, and 35 cause approximately 95% of cervical cancers.15,16 HPV-16 and HPV-18 cause approximately 50% of cervical-cancer precursors.17 The HPV life cycle occurs only in keratinocytes undergoing differentiation (Fig. 1). In most cases, infection occurs without malignant transformation. In such cases, the viral DNA is maintained separately from the host DNA as an episome. In the subgroup of HPV infections leading to malignant transformation, the viral DNA is often integrated into the host genome during progression of the cancer. Carcinogenesis is associated with the expression of proteins E6 and E7, which inactivate tumor