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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.E6 also has a close relationship with the cellular protein E6-associated protein (E6-AP), which is involved in the ubiquitin ligase pathway, a system that acts to degrade proteins.E6-AP binds ubiquitin to the p53 protein, thereby flagging it for proteosomal degradation.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.Immunological control is HPV type-specific, meaning an individual may become resistant to one HPV type while remaining susceptible to other types.In one study, infection by HPV types 2, 27, and 57 was found in people with warts, while infection by HPV types 1, 2, 63, and 27 was found in people with clinically normal skin.

E6 produces a protein (also called E6) that binds to and inactivates a protein in the host cell called p53.

HPV-associated cancers make up over 5% of total diagnosed cancer cases worldwide, and this incidence is higher in developing countries where it is estimated to cause almost half a million cases each year.

Some of the "early genes" carried by the HPV virus, such as genes E6 and E7, act as oncogenes that promote tumor growth and malignant transformation.

Such infections are associated with genital or anal warts (medically known as condylomata acuminata or venereal warts), and these warts are the most easily recognized sign of genital HPV infection.

The strains of HPV that can cause genital warts are usually different from those that cause warts on other parts of the body, such as the hands or feet, or even the inner thighs.

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