Human papillomavirus (HPV) infection
HPV infection is a necessary step in the development of virtually all precancerous and cancerous lesions. Epidemiologic studies convincingly demonstrate that the major risk factor for development of preinvasive or invasive carcinoma of the cervix is HPV infection, far outweighing other known risk factors.
More than 6 million women in the United States are estimated to be infected with HPV. Transient HPV infection is common, particularly in young women, while cervical cancer is rare. The persistence of an HPV infection leads to increased risk of developing precancerous and cancerous lesions.[4,5]
The strain of HPV infection is also important in conferring risk. There are multiple subtypes of HPV that infect humans; of these, subtypes 16 and 18 have been most closely associated with high-grade dysplasia and cancer. Studies suggest that acute infection with HPV types 16 and 18 conferred an 11-fold to 16.9-fold risk of rapid development of high-grade CIN.[6,7,8] Further studies have shown that infection with either HPV 16 or 18 is more predictive than cytologic screening of high-grade CIN or greater disease, and that the predictive ability is seen for up to 18 years after the initial test.[9,10,11]
There are two commercially available vaccines that target anogenital-related strains of HPV. The vaccines are directed towards HPV-naïve girls and young women, and although penetration of the vaccine has been moderate, significant decreases in HPV-related diseases have been documented. (Refer to the PDQ summary on Cervical Cancer Prevention for more information.)
Other risk factors
Other risk factors for cervical cancer include the following:
- High parity.
- Increased number of sexual partners.
- Young age at time of first sexual intercourse.
- Low socioeconomic status.
- History of smoking.
- Long-term use of oral contraceptives.
Given the relevance of HPV status in assessing risk, studies limited to HPV-positive women in cases and the control groups provide the most information on the additional cofactors that may promote progression of HPV infection to precancerous and cancerous lesions.
(Refer to the PDQ summary on Cervical Cancer Prevention for more information.)