Abstract
The human papillomavirus (HPV) comprises a heterogeneous group of double-strand DNA viruses with variable potential to infect human epithelial cells and trigger neoplastic transformation. Its 8kb genome encodes proteins required for virus replication and self-organized formation of infectious particles but also for early proteins E6 and E7 able to trigger neoplastic transformation. E6 and E7 of high-risk (HR) HPV subtypes can bind to p53 or release E2F and abrogate replication control. Due to variable amino acid sequence (AAS) in the binding sites of E6 and E7 particular HR-HPV variants within subtypes are essentially heterogeneous in efficacy triggering neoplastic transformation and cancer development. This could explain differences in the clinical course of HPV-driven head and neck cancer.
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