Clinical, subclinical, and latent human papillomavirus (HPV) infections are distinguished from HPV-associated neoplasia. Besides HPV additional cofactors are necessary to transform HPV infected tissue to intraepithelial or invasive neoplasia. Risk factors for the presence of HPV are high number of sexual partners, early cohabitarche, young age at first delivery, suppression and alteration of immune status, young age and hormonal influences. While the fact of a high number of sexual partners exclusively increases the risk of HPV infection, it is not known whether the other factors lead to either an increased risk for HPV infection and/or to HPV-associated neoplasia. Subclinical and latent genital HPV infections are highly prevalent. The prevalence rate depends on the sensitivity of the HPV detection system used, on age and sexual activity of the population screened, and on the number of subsequent examinations performed for each subject. Sexual transmission is the main pathway for genital HPV's, however, vertical, peripartal, and oral transmission are also possible. Seroreactivity against genital HPV may be due to an active infection or the result of contact with HPV earlier in life. Antibodies against the HPV 16 E7 protein indicate an increased risk for cervical cancer. Compared with humoral response cellular immune response is probably more important for regression of genital HPV infection: impaired cellular response is characterized by depletion of T helper/inducer cells and/or Langerhans cells and impaired function of natural killer cells and/or the infected keratinocyte. In condylomata replication and transcription of viral nucleic acids and antigen production coincide with cellular differentiation. However, the interaction between HPV and the keratinocyte on a molecular level in subclinical and latent disease is not well understood. Regression or persistence of subclinical and latent genital HPV infections as observed in longitudinal investigations show a constant come-and-go of HPV presence. Subclinical or latent cervical infections with high-risk HPV types (such as HPV 16 and 18) have an increased risk for the development of HPV-associated neoplasia.
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