Examining the Complex Relationship of Human Papillomavirus to Cervical Dysplasia and Carcinoma.

Abstract

Human papillomavirus (HPV) infection is quite common in women and is clearly the major risk factor for cervical intraepithelial neoplasia and invasive cervical cancer. HPV DNA has been detected in 80% to 90% of CIN 3 lesions and invasive cervical cancers. While the most common presentation is warts, or condylomata, many infections are detected only by Pap smear cytologic evidence. We still do not have a clear understanding of HPV latency, reactivation, subclinical infection without apparent disease, and the triggers or cofactors required for malignant transformation. More than 70 different strains of HPV have been identified, and specific subtypes have been associated with a greater risk of progression to dysplasia and cervical cancer. A better knowledge of the oncogenic mechanisms of HPV and improved diagnostic testing is critical to guide future therapeutic and preventive investigations. The Pap smear is used for initial screening; cytologic results suspicious for premalignancy or malignancy are subsequently evaluated by colposcopy and biopsy of suspicious lesions. Cervical cancer has been designated an AIDS-defining illness; in HIV-infected patients, the prevalence of HPV is 5 times that of the general population. Because the disease presents at a later stage in HIV-infected patients and is less responsive to treatment, close attention to timely Pap smears and appropriate follow-up is important in this population. Presently, early detection and aggressive treatment and follow-up of premalignant lesions offer the best approach to the prevention of cervical cancer.