High-risk human papillomaviruses can induce malignant transformation of cells resulting in anogenital cancers, particularly cervical cancer (CC), and a proportion of head and neck squamous cell carcinomas (HNSCC). The viral E6 and E7 oncoproteins are required for the induction and maintenance of transformation and the E5 protein contributes to tumorigenesis (1). The E6 and E7 expression is usually increased after the integration ofviral DNAinto the host genome which is associated with inactivation of the viral E2 gene (2).
InHNSCC and CC cases driven by HPV infection, analternative tumorigenesis pathway has been described with extrachromosomal persistence of the HPV genome and higher expression of the viral E2, E4,and E5 genes (3).