Table 1.

Possible molecular and cellular mechanisms inducing CRC.

Oncoviru	Evidence in CRC	Possible CRC-inducing mechanisms
HPV	•HPV positivity increases the CRC risk [115]	•HPV DNA integration into the host’s genome and cell transformation;
	•Persistent HPV infection is linked to anal and rectal cancer [116]	•HPV-encoded E5, E6, and E7 proteins may intervene in the neoplastic lesion onset [36]
MCPyV	•MCPyV DNA found in 90% of CRC samples analyzed, especially in lymphocytes [118].	•MCPyV-induced CRC might rely on the T-antigen-mediated inactivation of p53 and pRB, as well as other signaling pathways [119].
CMV	•CMV positivity tumors predicts low disease-free survival rate in CRC patients [121].	•It is likely to induce angiogenesis, resistance to apoptosis, cellular invasion, and metastasis [122]
EBV	•EBV positivity is associated with CRC pathogenesis [123]	•EBV DNA integration into the host’s genome [125]
	•In 20% of CRC cases a coinfection by both EBV and CMV (or HHV-6B) was observed [124]	•Alteration of DNA methylation pattern [125]
		•EBV nuclear antigens EBNA1 and 2 induce PIK3Ca mutations, DNA hypermethylation, JAK2 activation along with PD-L1 and PD-L2 overexpression [36].
HBV	• HBV seropositivity increase CRC risk [109]	•HBV-induced CRC might rely on the HBx-mediated inactivation of p53,stucking cells into the S-phase [36]