Table 1.

Induction of atherosclerosis and immunosenescence by different viruses.

Virus	Atherosclerosis	Immunosenescence	References
CMV	Expression of cytokines and chemokines Expresion of cellular adhesion molecules Proliferation and migration of VSMCs Molecular mimicry Inhibition of apoptosis Inflammatory reactions Endothelial injury Coagulation and thrombosis Lipid accumulation	Decreased frequency of naïve T cells Decreased expression of CD27 and CD28 Increased expression of KLRG-1 and CD57 Re-expression of CD45RA Production of granzyme B Induction of inflammaging	( 135–138 )
EBV	Secretion of pro-inflammatory cytokines Expression of ICAM-1 Proliferation of VSMCs Induction of blood monocytes Alteration in lipid metabolism	Replicative stress G1 phase cellular arrest DNA damage Alteration in metabolic pathways	( 139–143 )
HBV	Alteration in macrophage phenotype? Induction of chronic inflammation Induction of fatty acid oxidation	Increased expression of p16 INK4a and p21 G1 phase cellular arrest DNA damage	( 144–148 )
HCV	Increased production of IL-1β and TNF-α Induction of chronic inflammation Increased synthesis of MMP-9 Generation of ROS	Decreased expression of CD27 and CD28 Increased expression of KLRG-1 and CD57 Increased expression of TIM-3 and P16INK4a Telomere shortening	( 149–152 )
HIV	Production of inflammatory mediators Secretion of MCP-1/CCL2 chemokine Expression of adhesion molecules Activation the macrophage inflammasome Foam cell formation	Decreased CD4/CD8 ratio Increased CD28−CD8+ T cells Increased expression of TIM-3 and P16INK4a Increased levels of IL-6 and TNFα Decreased T cell repertoire T cell Telomere shortening	( 153–156 )
SARS-CoV-2	Cytokine storm Endothelial injury Thromboinflammatory response Alteration in lipid metabolism	Increased expression levels of p16, p21, SA-β-Gal in ECs SASP production	( 157–160 )