**5. Conclusions**

The SARS-CoV2 pandemic has sparked a brainstorming session over the underlying mechanisms of viral diseases. Many assumptions have been made. This chapter considers possible consequences of cholesterol depletion in the membranes of infected cells due to the formation of cholesterol-rich viral envelopes. At a high viral load and high replication rate the reduction in the cholesterol level in the cell membranes can lead to their permeabilization and subsequent cell death, and this can be one of the factors in pathogenesis of diseases induced by SARS-CoV2. Cholesterol-recognition/interaction (CRAC) motifs in viral proteins may represent a mechanism for the binding of the viral protein with cholesterol. Substances preventing these interactions of viral proteins with cholesterol can suppress the formation of the viral envelope and therefore can be studied as possible antiviral drugs. Peptides containing CRAC motifs from viral proteins may be among these substances.
