HSV upregulates lectin-like oxidized LDL receptor-1 (LOX-1), which is the major receptor protein of oxidized LDL (oxLDL), stimulates the uptake of oxLDL in endothelial cells, provokes lipid accumulation and its metabolism through the increased acquisition of saturated cholesteryl esters and triacylglycerols, induces the accumulation of coronary artery calcium, and causes the development of thrombosis, which are all related to the development of atherosclerosis [49,50,51,52]. The gene discussed is OLR1; the disease is atherosclerosis.