Abstract

Cervical cancer has been recognized as a rare outcome of a common, sexually transmitted infection whose etiologic association is restricted to a few human papillomavirus (HPV) types. With optimal testing systems HPV DNA can be identified in nearly all specimens of invasive cervical cancer, and it is claimed that infection of the cervix with HPV is a necessary cause of cervical cancer. The evidence is consistent worldwide for squamous cell carcinomas (SCC), adenocarcinomas, and the vast majority (>95%) of the immediate cervical cancer precursors, namely high-grade squamous intraepithelial lesions (HSILs)—also known as cervical intraepithelial neoplasia 3 (CIN 3) or carcinoma in situ. Cofactors that modify the risk for HPV DNA-positive women include the use of oral contraceptives (OCs) for 5 or more years, smoking, high parity (5 or more full-term pregnancies), and previ-ous exposure to other sexually transmitted diseases such as Chlamydia trachomatis and herpes simplex virus type 2 (HSV-2). Women exposed to the human immuno-deficiency virus (HIV) are at high risk for HPV infection, HPV DNA persistence, and progression of HPV lesions to cervical cancer.

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