Viral carcinogenesis, viral entry, and viral–host genome integration. Hallmarks of viral carcinogenesis from integration to malignant transformation for human oncoviruses, i.e., HPV, HBV, and HIV-1 (accelerates oncovirus-mediated carcinogenesis). Viral entry into mammalian cells is host- and surface-receptor-specific [4,11,12]. The modes of viral–host integration differ, respectively, among HPV, HBV, and HIV-1 to include faulty viral partitioning to daughter cells during mitosis, non-homologous end-joining (NHEJ). or micro-homology mediated end-joining (MMEJ) at double-strand DNA breaks, and provirus insertion [13,14,15,16,17,18,19]. cccDNA, covalently closed circular DNA; CCRS, chemokine receptor type 5; CXCR4, chemokine receptor type 4; DDR, DNA damage repair; dslDNA, double-stranded linear DNA; ECM, extracellular matrix; GFR, growth factor receptor; HSPG, heparin sulfate proteoglycan; NTCP, Na+-taurocholate co-transporting polypeptide; and rcDNA, relaxed circular DNA (figure created with BioRender.com).