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Keywordsinfectious cancer; human oncogenic viruses; transforming mechanisms; KSHV; microRNA; pathogenesis; human papillomavirus; tonsillar squamous cell carcinoma; base of tongue squamous cell carcinoma cancer; clinical outcome; oral HPV prevalence; polyomavirus; microRNA; inflammation; autophagy; glucose; therapy; exosomes; adenovirus; E4orf4; protein phosphatase 2A (PP2A); Src kinase; actin; Ynd1; Golgi UDPase; Acf1; SNF2h; cell-death; cell cycle; chromatin remodeling; adenovirus; E4-ORF3; transcription; cellular gene expression; HPV; papillomavirus; replication; DNA damage response; homologous recombination; keratinocyte; replication foci; DNA repair; partitioning; episome; high-risk human papillomavirus; keratinocyte; immune evasion; DNA damage; DNA repair; human tumour viruses; HPV; MCPyV; HTLV-1; EBV; KSHV; HBV; HCV; oncogenic viruses; host cell receptors; viral attachment; entry mechanisms; Kaposi’s sarcoma-associated herpesvirus; KSHV; DNA damage response; DDR; lytic replication; ATM; ATR; DNA-PK; n/a; HPV16 E7; SELEX; RNA aptamers; cell surface localisation; ER retention; HPV; E6; PDZ; 14-3-3; cell polarity; CTCF; DNA virus; gene expression; cohesin; chromatin organization; human papillomavirus; tropism; diversity; evolution; tissue stem cells; niche; carcinogenesis; human papillomavirus (HPV); virus; native virions (NV); virus-like particles (VLPs); pseudovirions (PsV); quasivirions (QV); Wnt/β-catenin; HPV E6 and E7 oncoproteins; HPV-related cancers; head and neck squamous cell carcinoma; high risk HPV; HPV-related oropharyngeal squamous cell carcinoma; cancer treatments; target therapy; HNSCC; HR HPV; OPSCC; human papillomavirus (HPV); E6 oncoprotein; Connexin 43 (Cx43) trafficking; human homologue of Drosophila discs large (hDlg)
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