Direct viral infection of endothelial cells is not a prerequisite for senescence induction, as inflammatory cues and oxidative stress, as well as some specific molecules, such as endothelin-1 (ET-1), SARS-CoV-2 spike protein, leukocyte microparticles, angiotensin II, homocysteine, cytokines, and others [79, 84–87], have the potential to induce endothelial senescence. This evidence concerns the gene EDN1 and viral infectious disease.