Moreover, viral infection of endothelial cells did not cause an increase in adhesion molecules (E-selectin, ICAM-1 and VCAM-1), but infection of epithelial cells resulted in increased E-selectin and VCAM-1, suggesting that the endothelial damage observed in COVID-19 is initiated by a cytotoxic effect from neighboring infected pulmonary epithelial cells. This evidence concerns the gene VCAM1 and viral infectious disease.