According to our study results, endothelial dysfunction could therefore be a complementary mechanism for the detrimental effects of viruses on atherosclerosis through the production of pro‐inflammatory cytokines such as IP‐10, IL6 and IL‐8, and expression of cell adhesion molecules VCAM‐1 and ICAM‐1 upon MDA‐5 stimulation. This evidence concerns the gene CXCL8 and endothelial dysfunction.