[HPV and skin neoplasia]

Human papillomaviruses (HPV) induce benign and malignant tumors of skin and mucosa. Non-melanoma skin cancer (NMSC) is the most frequent malignancy in fair-skinned populations, particularly frequent in countries with high sun exposure and in immunosuppressed patients. The high prevalence of Beta-HPV in skin tumors renewed interest in a possible etiologic role of HPV. In contrast to cervical cancer, the presence of HPV is probably not mandatory for maintenance of the malignant phenotype of skin cancer cells, since only low copy numbers of HPV DNA persist in skin cancers. Higher viral loads in actinic keratoses are compatible with a carcinogenic role of cutaneous HPV in early phases of NMSC development. There is some evidence from case-control studies for an increased risk of cutaneous squamous cell carcinoma related to beta-HPV infection. HPV8 is clearly carcinogenic in transgenic mice. At the molecular level, oncogenic activities of beta-HPV have been attributed to effective inhibition of apoptosis and interference with DNA repair pathways by viral E6 proteins. In addition E7 proteins deregulate the cell cycle and enhance invasive growth.