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Prevention of Genital Human Papillomavirus Infection
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Epidemiology of Genital HPV Infection

Incidence and Prevalence of Genital HPV Infection
Accurately assessing the extent of genital HPV infection in the U.S. population has been difficult for many reasons. Data on prevalence and incidence of HPV infection are limited because there is no routine screening for HPV infection, and it is often unclear whether a newly diagnosed infection is recently acquired or longstanding. Neither HPV infection nor genital warts are routinely reported to state health departments for the following reasons: (a) no standard justification for recommending STD case reporting (e.g., patient care measures such as curative treatment for patients and their sex partners, or monitoring ongoing prevention programs) exists for genital HPV infection or warts, (b) most infections clear spontaneously, and (c) case reporting would create a large burden for providers, health departments and laboratories given the high prevalence of infection (14).

Cases of cervical cancer are routinely reported to cancer registries such as the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) program, and Centers for Disease Control and Prevention (CDC)-supported state cancer registries. However, because cervical cancer is a rare and late manifestation of HPV infection, cancer surveillance provides limited information on the burden and current trends of HPV infections. CDC is conducting a survey of the general U.S. population and a survey of women attending different types of clinics to improve measures of the prevalence of genital HPV. Results for the U.S. population survey will be available in late 2005, and, for the clinic based survey, in 2007. Data from these studies will be useful in evaluating the impact of future prevention strategies on HPV prevalence.

Because of the above issues, the magnitude of genital HPV infection is derived from extrapolations of epidemiologic studies. Studies that detect HPV DNA measure current infection, and studies that detect HPV antibodies using blood tests provide approximations of lifetime infection. Overall, in the United States, an estimated 20 million people (15% of the population) are currently infected with HPV, 50–75% of which is with high-risk types, and about 5.5 million people are infected every year (1). It has been estimated that at least 50% of sexually active men and women acquire genital HPV infection at some point in their lives; a recent estimate suggests that 80% of women will have acquired genital HPV by age 50 (15;16). An estimated 9.2 million sexually active adolescents and young adults 15 to 24 years of age are currently infected with HPV (17).

Prevalence studies in the United States have primarily included convenience samples of women attending managed care, STD, or university clinics. Studies have found that the prevalence of HPV infection is lowest in women who have never had sexual intercourse (18-21). Genital HPV infection is especially common among sexually active young women (less than 25 years of age), with prevalence decreasing with older age (22-30). While results vary by population studied, and sampling and detection methods used, overall they indicate that prevalence of genital HPV infection in sexually active young women in the United States ranges from 17–84% (22-29); most studies have reported a prevalence greater than 30% (22;23;25-27). In a study conducted in Portland, Oregon, 32% of young women ages 16 to 24 years had genital HPV DNA detected versus only 4% of women ages older than 45 years (24). The higher rates in younger women appear to be related to transmission of new infection during the early years of sexual activity, with infection clearing over time in most women (28;31). By far, the most common infections are with the high-risk types. Infection with multiple types of HPV occurs in approximately 5–30% of infected women (23;32-34). HPV infection is most likely to be detected in women who have cervical cancer precursors; in one study, over 85% of women with cervical cancer precursors had detectable HPV DNA (34).

These findings are supported by studies of incident (new) genital HPV infections, which can more accurately determine rates, as well as behavioral risk factors for infection. Studies of HPV incidence have been conducted in a variety of settings with variable follow-up periods. Incidence of HPV infection in college women studied for two to three years was 32–43% (21;28). Other studies assessing populations of women using routine gynecological or family planning services found incidences of 11–32% in one year, and 44–55% in three years (29;31;33;35;36). The incidence of high-risk types, such as HPV-16, is higher than the incidence of low-risk types (28;29;31). For example, in one study, the incidence in one year was 32% for high-risk HPV types compared with 18% for low-risk HPV types (29).

The risk factors consistently associated with HPV infection in women are young age (age less than 25 years) and sexual behavior, specifically number of sex partners, as described below (Transmission and Prevention of Genital HPV, page 11). Other risk factors identified include early age of first sexual intercourse, and male partner sexual behavior. Less consistently identified risk factors include smoking, oral contraceptive use, nutritional factors, and lack of circumcision of male partners (20). Many of the identified risk factors are likely markers for unmeasured sexual behavior (21;25;37-39). In addition, immune suppression is associated with HPV detection. Studies in women with HIV infection, undergoing dialysis, or after kidney transplant, demonstrate that HPV detection is particularly common with immune suppression (17;40-43).

The prevalence of genital HPV infection in men is more difficult to assess because it is not clear which are the optimal anatomic sites or specimens to test. Most published studies have been conducted outside the United States, in men attending STD or university clinics, or among male partners of women with HPV infection. HPV DNA can be detected at various anogenital sites, including the penis, urethra, scrotum, or anus, as well as in urine and semen (44-56). In heterosexual men, infection is most commonly detected on the penis (54-57). A recent study that evaluated HPV DNA in the distal penis (urethra, glans, coronal sulcus, foreskin) documented higher prevalence of infection in uncircumcised men than in circumcised men (19.6% vs. 5.5%) (46). Prevalence of genital HPV infection in heterosexual men in the populations studied ranges from 16–45%; detection is highly dependent on the anatomic sites or specimens tested (e.g., urine, semen) (45;46;49;52). Risk factors for HPV detection in men include greater lifetime number of sex partners, number of recent sex partners, being uncircumcised, or current genital warts (45;46;52). The relationship of young age with HPV detection is not as consistent in men as in women (45;49;52).

HPV serologic (blood) tests that detect antibodies to the outer proteins of HPV have been useful in assessing previous HPV infection. They complement the studies that are based on HPV DNA detection because HPV DNA is not persistently detectable in most infected people. However, these tests likely underestimate the true extent of previous infection because only 50–70% of persons with detectable HPV DNA develop antibodies (58-60). A recently completed study of the U.S. population conducted by CDC showed that 18% of women and 7% of men aged 12 to 49 had antibodies to HPV-16 (61). The strongest predictors of antibody positivity in both women and men were various measures of past sexual activity, including lifetime number of partners. Antibody prevalence is substantially higher in populations with greater sexual activity. For example, a study of patients attending a U.S. STD clinic found HPV-16 antibody prevalence rates of 55% in women and 33% in men (62).

Prevalence of Sequelae of Genital HPV Infection
Estimates for genital warts are relatively imprecise; however, limited data suggest that each year in the U.S. as many as 100 per 100,000 persons develop genital warts (63), and 1.4 million currently have genital warts (about one percent of the sexually active U.S. population) (64). Rarely, genital HPV infection with low-risk types may be transmitted from mother to baby during delivery resulting in respiratory tract warts in the baby, an illness known as recurrent respiratory papillomatosis (RRP). Estimates of the incidence rate for RRP are also relatively imprecise, but range from 0.4 to 1.1 cases per 100,000 children (65).

Rates of cervical cancer have fallen by approximately 75% since the introduction of Pap testing programs. Cervical cancer incidence in the U.S. is currently estimated to be 8.3 per 100,000 women, with approximately 12,200 new cases and 4,100 deaths occurring annually (66).

Natural History of Genital HPV Infection
Most HPV infections are transient and asymptomatic, causing no clinical problems. Studies have shown that 70% of new HPV infections clear within one year, and as many as 91% clear within two years (28;33;67;68). The median duration of new infections is typically eight months (28;67). HPV-16 is more likely to persist than other HPV types (28); however, most HPV-16 infections become undetectable within two years (28). Factors associated with persistence include older age, high-risk HPV types, infection with multiple HPV types, and immune suppression (69;70). The gradual development of an effective immune response is thought to be the likely mechanism for HPV DNA clearance.

HPV infection that persists is the most important risk factor for cervical cancer precursors and invasive cervical cancer (15;67;69-71). A recent study found that the risk for developing cervical cancer precursors was 14 times higher for women who had at least three positive tests for high-risk HPV compared with that for women who had negative tests (68). However, most women with persistent HPV infection do not develop low-grade cervical cell abnormalities, cervical cancer precursors or cervical cancer (28;31;68;72).

Skin and mucosal changes caused by genital HPV infection --both genital warts and cervical cell abnormalities-- often go away without treatment, probably as a result of the development of an effective immunologic response. Rates of spontaneous clearance and progression to cancer without treatment vary for low-grade and high-grade cervical cell abnormalities. Low-grade cervical cell abnormalities usually clear spontaneously (60% of cases) and rarely progress to cancer (1%), while high-grade cervical cell abnormalities have lower rates of spontaneous clearance (30–40%) and much higher rates of progression to cancer without treatment (greater than 12%) (73).

In addition to persistent infection with high-risk types of genital HPV, other co-factors appear to be necessary for the development of cervical cancer (74). Factors such as long-term use of oral contraceptives, a high number of live births, and immune suppression have been found in some studies to be associated with cervical cancer (74-81). In addition, recent studies have demonstrated that co-infection with Chlamydia trachomatis or herpes simplex virus type-2 (HSV-2), the cause of genital herpes, may increase the risk of both cervical cancer precursors and cervical cancer (81;82).

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