Abstract

Human papillomaviruses (HPVs), of which there are more than 200 types, infect epithelial cells of the skin and mucosal surfaces by direct contact and, as a whole, are fairly ubiquitous in the human population. These viruses are intraepithelial pathogens that enter but do not kill the host cell and have evolved numerous mechanisms to evade the host immune system. Of clinical significance, over five percent of human cancers are initiated by infection with HPV. These include cervical, oropharyngeal, anal, penile, vulvar, and vaginal cancers, which are driven by sexually transmitted HPVs, types 16 and 18. The incidence of cervical cancer, the most common women’s cancer worldwide, has decreased in the western world following widespread implementation of expensive “Pap” screening programs paired with early clinical intervention. Certain HPV-driven cancer types are however on the increase, including oropharyngeal and anal cancers, especially in men. Additionally, a significant fraction of cutaneous squamous cell carcinomas (cSCC) and basal cell carcinomas (cBCCs) are associated with HPV 5 infection or with the dozen or so other cancer-causing HPV types (1,2).

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