Abstract
Epidermodysplasia verruciformis (EV) is characterized by a clinically distinctive pattern of beta-HPV induced flat warts that may evolve into epithelial skin cancers. The current understanding is that EV encompasses two etiological situations: Classic, inherited type EV (IEV), beginning in childhood or adolescence, due to Trans Membrane Channel (TMC) - 6 and 7 (EVER-1 and 2) gene mutations 75% of patients, or to alterations resulting in T-Cell immune deficiencies (IDs) on Ras Homolog Family Member H (RHOH), Coronin 1A (CORO 1A), Macrophage Stimulating factor 1 (MST-1), or interleukin 7 (IL7) genes.
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