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    Update: HPV prevention

    Human papillomavirus (HPV) infection is associated with virtually all cervical cancers, as well as with more than 90% of anal cancers, 65% of vulvar and vaginal cancers, 35% of penile cancers, and 70% of head and neck cancers. It is also the causative agent of benign genital warts.1-6 HPV is the most common sexually transmitted infection, with a worldwide point prevalence of 11.7%,7 and an estimated lifetime prevalence of 80%–90% in both women and men by age 45.8 Approximately 14.1 million incident HPV infections occur in the United States each year.9

    Related: HPV vaccine rates, race, and income

    In the past decade, the prevention of HPV-related disease became a public health priority. In 2006, a quadrivalent vaccine (Gardasil) became the first commercially available HPV vaccine, targeting high-risk HPV serotypes 16 and 18, which alone account for 70% of cervical cancers,10 as well as low-risk serotypes 6 and 11, which are predominantly responsible for genital warts. A bivalent vaccine (Cervarix) was released in 2007 in Europe and in 2009 in the United States, and targets high-risk types 16 and 18. More recently, Gardasil 9 was licensed for use by the Food and Drug Administration (FDA) in December 2014. This newest vaccine targets the 7 most common cancer-causing subtypes (16, 18, 31, 33, 45, 52, and 58), which account for more than 90% of HPV-related cancers,11 as well as subtypes 6 and 11. It is hoped that widespread use of these vaccines will significantly reduce the number of women and men who develop HPV-related disease.

    Biology and natural history of HPV infection

    More than 40 of the 100+ distinct types of HPV are known to infect the genital and oral mucosa. Infections with low-risk types like 6 and 11 can cause low-grade cervical cell changes, genital warts, and recurrent respiratory papillomatosis. Fifteen known high-risk HPV types—16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82—are classified as carcinogens implicated in development of many cancers.12

    HPV has a high infectivity rate, with an estimated 40%–60% probability of transmission per coital act.13 The virus is introduced into the body through microabrasions on mucosal surfaces and infects the basal layer of the epithelium. After infection, epithelial cells that are normally non-dividing remain in an active cell cycle. This can result in a thickened, sometimes exophytic, epithelial lesion. The virus is released as cells exfoliate from the epithelium. In precancerous lesions, the viral DNA is integrated into the human genome. Because of integration, the E6 and E7 genes are constitutively expressed in HPV-positive cervical cancer; these oncogenes can manipulate cell cycle regulators, induce chromosomal abnormalities, and block apoptosis.14

    Most HPV infections, whether with low- or high-risk subtypes, are cleared by the body's immune system. For cervical HPV, the median duration of infection is 8 months;15 70% of infections are cleared by 1 year and up to 90% are cleared in 2 years. Continuing infection progresses slowly through dysplastic phases over the course of several years, with up to 15% of high-grade squamous intraepithelial lesions progressing to invasive cervical cancer in 5 to 10 years (range 1–20 years). 16

    NEXT: Vaccine immunogenicity

    Soledad Jorge, MD
    Dr Jorge is a resident in Obstetrics and Gynecology at Columbia University College of Physicians and Surgeons and New York Presbyterian ...
    Jason D Wright, MD
    Dr Wright is Chief of the Division of Gynecologic Oncology in the Department of Obstetrics and Gynecology, Columbia University College ...


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