Table 1: Strategies Used by Tumors and CMV for Immune Escape

Strategy	Tumors	Ref.	CMV	Ref.
Impairment in Antigen Processing and Presentation
Impairment in surface expression of MHC-I	MHC-I gene mutations, inhibition of MHC-coding genes expression, impairment in antigen binding or peptide transport from the endoplasmic reticulum to the cell surface	[23]	Directly acting on MHC-I molecules or by acting on MHC-I associated proteins, including TAP and tapasin	[25, 27]
Escape from Natural Killer Cells
NK activating receptors	Immune surveillance of cancer through NKG2D/ NKG2DLs pathway	[32]	Retention of ligands of NKG2D (MICB, ULBP1 and 2) in ER by gpUL16	[54, 55]
	Regulation of MICB by cellular miRNA	[64]	Down regulation of MICB by HCMV miR-UL112	[57]
	Intercellular retention of MICA inhibits NK cytotoxicity	[42]	Inhibition and intracellular retention of MICA by UL142	[56, 59]
	Immune surveillance through Natural Cytotoxicity Receptors NKp30, NKp44, NKp46, and NKp80	[32, 33]	Reduced NKp30-mediated killing by pp65	[63]
	Anti-tumor response by DNAM-1	[36, 37]	Down-regulation of CD155 expression, a ligand for DNAM-1, by gpUL141	[60]
NK Inhibitory receptors	Blockade of the inhibitory receptors LIR-1 and NKG2A results in increased NK cell cytotoxicity	[44]	gpUL18 binds with LIR-1 and inhibits LIR-1 + NK cell activity	[47, 48]
	Expression of “non classical” HLA-E induces a decrease in NK responses through interaction with CD94/NKG2A	[24]	Over expression of HLA-E by gpUL40	[52, 53]
Blockade of Death Receptors-Mediated Apoptosis
Over-expression of antiapoptotic proteins	Over-expression of FLIPL,S which act as caspase 8 inhibitors	[67]	Expression of FLIP by immediate early 2 (IE2) protein	[84]
	Over-expression of the anti-apoptotic protein Bcl-2	[70]	Over-expression of Bcl-2 in HCMV infected cells	[10, 85]
	Over-expression of other antiapoptotic Bcl-2 family members such as Bcl-x or Mcl-1	[74, 75]
Inhibition of pro-apoptotic molecules and death receptors	Decreased expression of Fas Mutations or deletions in genes encoding Fas and TRAIL-R1-R2	[76] [77]	Inhibition of recruitment of pro-caspase 8 to the Death-inducing Signaling Complex (DISC) by product of HCMV UL36 gene	[87]
			Inhibition of proapoptotic Bcl-2 family members Bax and Bak by product of the HCMV UL37 gene	[86]
Escape from Complement Attack
Complement Regulatory Proteins (CRPs)	Expression of CRPs (CD46, CD55, CD59, and CD35) was noticed in a wide range of cancer cells	[91-93]	HCMV upregulates expression of host-encoded CRPs resulting in protection from complement-dependent lysis	[96, 97]
			HCMV incorporates host cell-derived CRPs, CD55 and CD59 into its virions	[98]
Immune Tolerance Establishment
Expression of interleukin-10	Increased release of IL-10 in cancers, conferring a more invasive phenotype	[102-108]	HCMV encodes an IL-10 homolog (cmv-IL-10) that shares human IL-10 immunomodulatory properties	[114- 118]
Expression of TGFβ	Overexpression of TGFβ promoted tumor-immune escape and was associated with tumor progression with worse prognosis.	[128-131, 134-136]	HCMV induced transcription and release of TGFβ	[138-140]