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All HPVs are believed to be capable of establishing long-term "latent" infections in small numbers of stem cells present in the skin.

In such cases, in vitro studies suggest that the E6 protein of the HPV virus may inhibit apoptosis induced by ultraviolet light.Furthermore, HPV can induce a tumorigenic process through integration into a host genome which is associated with alterations in DNA copy number.E6 produces a protein (also called E6) that binds to and inactivates a protein in the host cell called p53.Most HPV infections of the cervix are cleared rapidly by the immune system and do not progress to cervical cancer (see below the Clearance subsection in Virology).Because the process of transforming normal cervical cells into cancerous ones is slow, cancer occurs in people having been infected with HPV for a long time, usually over a decade or more (persistent infection).Throat cancers associated with HPV have been estimated to have increased from 0.8 cases per 100,000 people in 1988 to 2.6 per 100,000 in 2004.

Researchers explain these recent data by an increase in oral sex.In the United States, HPV is expected to replace tobacco as the main causal agent for oral cancer, and the number of newly diagnosed, HPV-associated head and neck cancers is expected to surpass that of cervical cancer cases by 2020.In recent years, the United States has experienced an increase in the number of cases of throat cancer caused by HPV type 16.Most people acquire genital HPV infections at some point in their lives, and about 10% of women are currently infected.A large increase in the incidence of genital HPV infection occurs at the age when individuals begin to engage in sexual activity.Genital warts are quite contagious, while common, flat, and plantar warts are much less likely to spread from person to person.

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