EPIDEMIOLOGY OF ANOGENITAL HPV INFECTION

The latency period of anogenital HPV infection is extremely variable; usually 3–6 months, but latency periods of many months or even decades have been reported.(2) Evidence for such extended latency periods is seen in immunocompromised and normal patients who, despite having been sexually inactive for many years, can suddenly develop warts or cervical abnormalities. It is important to emphasise that developing genital warts during a long-term relationship does not necessarily imply the presence of other sexual contacts.

Epidemiology in females

Generally speaking the same HPV genotypes cause cervical cancer everywhere in the world with very little variation from region to region.(3) There is no evidence of a significant population based or genetic predisposition for cervical cancer. This means that risk is directly related to amount and timing of exposure to HPV infection, the likelihood of persistence and access to preventative health care. 10.5% of women worldwide are positive for HPV DNA in the cervix.(4) Smoking is an independent risk cofactor which may increase the risk of the development or progression of lesions once HPV infection has occurred. In an international meta analysis, the highest prevalence is in young women (20–25% around age 20) falling to 10% at age 30 and falling slightly thereafter,(5) while a study in the United Kingdom reported a prevalence of 40% in 20-24 year olds falling to 7% by 50 years of age.

Rates of HPV infection in young women are high following first sexual contact. 28% after 1 year with one sexual partner, increasing to 49% after 36 months, and remaining high with the acquisition of each new partner.(6,7)

Most HPV infection occurs after initiation of sexual activity and is transient, although in some cases HPV infection remains latent and may reactivate years later.(8) There is a rapid loss of detectable HPV in the first 6–12 months, with 80–90% becoming undetectable by 2 years. The key step in cervical carcinogensis is overt measurable hrHPV persistence, which after a year or two strongly increases the risk of the development of high grade CIN or AIS.(9,10) Some infections may become quiescent (latent) or undetectable (11) however, the fraction of HPV infections that become latent is unknown. In older women, detection of new HPV infection is likely to represent reactivation of infection rather than acquisition of a new, recent infection.(12,13) Reactivation is also proposed as a main source of newly detected HPV infection in HIV-positive and immunocompromised women who reported no new sexual partners.(14)

Studies of anal HPV infection in women suggest that it is far more common than originally thought.(15-17) Women with a history of vulval or cervical high-grade SIL or cancer are also at increased risk of anal HPV infection and HPV-related disease. In these studies anal intercourse was not a consistent risk factor with either anal HPV infection or anal SIL.(18)