Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States. The relationship of cervical cancer and sexual behavior was suspected for more than 100 years and was established by epidemiologic studies in the 1960s. In the early 1980s, cervical cancer cells were demonstrated to contain HPV DNA. Epidemiologic studies showing a consistent association between HPV and cervical cancer were published in the 1990s
Human papillomaviruses are small, double-stranded DNA viruses that infect the epithelium. More than 100 HPV types have been identified; they are differentiated by the genetic sequence of the outer capsid protein L1. Most HPV types infect the cutaneous epithelium and cause common skin warts. About 40 types infect the mucosal epithelium; these are categorized according to their epidemiologic association with cervical cancer.
Infection with low-risk, or non-oncogenic types, such as types 6 and 11, can cause benign or low-grade cervical cell abnormalities, genital warts and laryngeal papillomas. High-risk, or oncogenic, HPV types act as carcinogens in the development of cervical cancer and other anogenital cancers.
High-risk types (currently including types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, 73, 82) can cause low-grade cervical cell abnormalities, high-grade cervical cell abnormalities that are precursors to cancer, and anogenital cancers. High-risk HPV types are detected in 99% of cervical cancers. Type 16 is the cause of approximately 50% of cervical cancers worldwide, and types 16 and 18 together account for about 70% of cervical cancers.
● Most HPV infections are asymptomatic and result in no clinical disease
● Clinical manifestations of HPV infection include:
■ anogenital warts
■ Recurrent respiratory papillomatosis
■ Cervical cancer precursors (cervical intraepithelial neoplasia)
■ Cancer (cervical, anal, vaginal, vulvar, penile, and oropharyngeal cancer)
Risk factors for HPV infection are primarily related to sexual behavior, including lifetime and recent sex partners. Results of epidemiologic studies are less consistent for other risk factors, including young age at sexual initiation, number of pregnancies, genetic factors, smoking, and lack of circumcision of male partner.
HPV transmission can be reduced but not eliminated with the use of physical barriers such as condoms. Recent studies demonstrated a significant reduction in HPV infection among young women after initiation of sexual activity when their partners used condoms consistently and correctly. Abstaining from sexual activity (i.e., refraining from any genital contact with another individual) is the surest way to prevent genital HPV infection. For those who choose to be sexually active, a monogamous relationship with an uninfected partner is the strategy most likely to prevent future genital HPV infections.
● HPV4 (Gardasil, Merck)
■ approved for females and males 9 through 26 years of age
■ contains types 16 and 18 (high risk) and types 6 and 11 (low risk)
● a 9-valent vaccine licensed in December 2014
● HPV2 (Cervarix, GlaxoSmithKline)
■ approved for females 9 through 25 years of age
■ contains types 16 and 18 (high risk)
HPV Vaccine Efficacy
● High efficacy among females without evidence of infection with vaccine HPV types
● No evidence of efficacy against disease caused by vaccine types with which participants were infected at the time of vaccination
● Prior infection with one HPV type did not diminish efficacy of the vaccine against other vaccine HPV types