Natural history and epidemiological features of genital HPV infection.

The spectrum of genital HPV infections comprises clinical, subclinical, and latent disease in addition to HPV-associated neoplasia. The definition of subclinical and latent HPV infection is still incomplete and awaits clarification by highly sensitive HPV detection systems that preserve the morphology of the tissue. Genital HPVs infect the human body mainly by sexual transmission, but other pathways of HPV transmission may be possible as suggested by (a) high prevalences of antibody reactivity in children; (b) lack of association of HPV seropositivity with sexual activity; (c) presence of HPV DNA in oral cavity scrapings of children and adults; and (d) development of recurrent respiratory papillomatosis among children exposed to HPV 6 or 11 during birth. Successful infection depends on the infection site and the immunological state of the host: susceptibility to genital HPVs seems highest for the squamous epithelium of the lower genital tract. HPV DNA is also present in extragenital sites but this is rarely accompanied by clinical or subclinical lesions. The molecular basis for this specific tropism is unknown. The immune response in HPV-infected tissues is characterized by depletion of T helper/inducer cells or Langerhans cells and an impaired immunological function of natural killer cells or the infected keratinocyte. Epidemiological studies indicate that individuals with cell-mediated immunodeficiencies are at increased risk for genital HPV infections. Data about the biological course of genital HPV infections are just beginning to emerge. Regression or persistence of subclinical and latent genital HPV infections as analysed in longitudinal investigations show a constant come-and-go of HPV presence. In an infected individual, complete clearing of the virus seems rather exceptional. With respect to progression, the biological potential of cervical HPV infections is characterized by an increased risk for development of HPV-associated neoplasia, especially in lesions infected with high-risk HPV types (e.g., HPV 16 and 18). Demographic data of genital HPV infections are very variable due to differences in the HPV detection assays used and in the populations examined; the prevalence of subclinical and latent genital HPV infections appears to be at least three times higher compared with clinical HPV infections. This rate increases by a further 3-5-fold when patients are examined several times. Seroreactivity against genital HPV types may be due to an active infection or the result of contact with HPV earlier in life.(ABSTRACT TRUNCATED AT 400 WORDS)