“…On the basis of epidemiologic data regarding the behaviour of the viral lesions, HPV have been also divided in two groups: those at "high risk" oncogenic [High Risk (HR) -HPV genotypes like 16-18-31-33-35, 39,45,51,52,53, 56,58,59, 66, 67,70,73,68, 82), associated with potentially and overtly malignant lesions (anogenital cancers, giant condyloma of Bruschke and Lowenstein) and those at "low risk" oncogenic [Low Risk (LR)-HPV genotypes like 2, 4, 27 (the skin types) and mucosal types 6,11,13,32,42), more commonly associated with benign diseases (ordinary wart, condyloma, focal epithelial hyperplasia, squamous cells papilloma, Bowen's papillomatosis) [39][40][41][42][43]. After entry to host cell, HPV infection can manifest in two clinical states: 1) subclinical or unapparent infection, that is the silent presence of viral genome into inoculation site without any clinical and/or histological and/or cytological alterations of cervical mucosa [44]; 2) clinical infection, expression of proliferation of infected keratinocytes and associated with clinical and histological lesions of cervical mucosa. These lesions are usually benignant (e.g.…”