The severity of the current Coronavirus pandemic is not uniform worldwide. The reason for this differences may be explained in terms of either the difference in the immunity of different populations or the difference in the virulence of the virus in different parts of the world.
Enveloped viruses, like Coronavirus, enter their host cells, by first coming in contact with their specific receptors, and then fusion of their envelope with the plasma membrane of host cells. After replicating inside, they exit from their host cells by incorporating part of their host cell plasma membrane, and they further infect other cells. Both entry and exit take place in special areas of the plasma membrane known as lipid rafts which are micro-domains rich in cholesterols and sphingomyelins. It has been shown in virology labs that change in cholesterol content or lipid rafts on the cell membrane of the host cell can affect viral infectivity. Statins, by chronically depleting the endogenous cholesterol synthesis inside the cells, results in the activation of the negative feedback system, mediated by sterol regulatory element-binding proteins (SREBP) that act to increase cholesterol by upregulation of low-density lipoprotein receptors (LDL-R) in the plasma membrane of the cells. This could result in an increased uptake of cholesterol from the low-density lipoprotein (LDL) in the blood plasma. This, in turn, may result in a buildup of more lipid rafts that may enhance viral entry and also produce viruses rich in cholesterol in their envelope making them more stable in the external environment for a longer duration of time.
Keywords: Corona virus, Enveloped virus, Lipid rafts, Cholesterol, Statin, Sterol regulatory element-binding proteins (SREBP), Low-density receptor (LDL-R)