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Cervical Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI] - Evidence of Benefit

Human Papillomavirus

Epidemiologic studies to evaluate risk factors for the development of squamous intraepithelial lesions (SIL) and cervical malignancy demonstrate conclusively a sexual mode of transmission of a carcinogen.[1] It is now widely accepted that human papillomavirus (HPV) is the primary etiologic infectious agent.[2,3,4] Other sexually transmitted factors, including herpes simplex virus 2 and Chlamydia trachomatis, may play a cocausative role.[1] The finding of HPV viral DNA integrated in most cellular genomes of invasive cervical carcinomas supports epidemiologic data linking this agent to cervical cancer;[5] however, direct causation has not been demonstrated. More than 80 distinct types of HPV have been identified, approximately 30 of which infect the human genital tract. HPV types 16 and 18 are most often associated with invasive disease. Characterization of carcinogenic risk associated with HPV types is an important step in the process of developing a combination HPV vaccine for the prevention of cervical neoplasia. In a population-based study of HPV infection and cervical neoplasia in Costa Rica, 80% of high-grade squamous intraepithelial lesions (HSIL) and invasive lesions were associated with HPV infection by one or more of 13 cancer-associated types.[6] In this study, the risk of about half of HSIL and invasive cervical cancer was attributable to HPV-16. HPV-18 was associated with 15% of invasive disease but only 5% of HSIL, suggesting that HPV-18 may have a role in more aggressive cases of cervical malignancy.

Barrier methods of contraception are associated with a reduced incidence of SIL presumptively secondary to protection from sexually transmitted disease.[7,8] The effectiveness of condom use for the prevention of HPV infections has been evaluated in a prospective study of women aged 18 to 22 years who were virgins.[9] The number of vulvovaginal HPV infections was reduced with consistent condom use, and HPV infection rate was 37.8 infections per 100 patient-years among women whose partners used condoms 100% of the time in the 8 months before testing, compared with 89.3 infections per 100 patient-years among women whose partners used condoms less than 5% of the time (P trend = .005). No cervical SIL were detected among women reporting 100% condom use by their partner.[9]

Given the etiologic role of HPV in the pathogenesis of cervical neoplasia, vaccines to immunize against HPV infection would offer a primary prevention strategy for cervical cancer. A quadrivalent (HPV 6, 11, 16, and 18) vaccine using a late protein L1 construct to induce antibody-mediated immunity was approved for use by the U.S. Food and Drug Administration in 2006; a bivalent (HPV 16, 18) vaccine was approved in 2009.

Vaccine to prevent HPV infection

Persistent infection with oncogenic types of HPV such as HPV-16 and HPV-18 is associated with the development of cervical cancer.[10] A vaccine to prevent HPV infection with oncogenic-type viruses has the potential to reduce the incidence of cervical cancer. A vaccine against HPV-16 using empty-viral capsids called virus-like particles (VLP) was developed and tested for efficacy in preventing persistent infection with HPV-16.

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WebMD Public Information from the National Cancer Institute

Last Updated: February 25, 2014
This information is not intended to replace the advice of a doctor. Healthwise disclaims any liability for the decisions you make based on this information.
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