**Author details**

*Management of Dyslipidemia*

**5. Conclusions**

substances.

**Acknowledgements**

**Conflict of interest**

(project no. 18-04-01363).

cholesterol transporters [113–116], which can redistribute cholesterol from endogenous and/or exogenous sources. The use of cyclodextrins increased the lifespan of NPC1−/− experimental mice [117] and improved the condition of patients with Nieman–Pick disease [118]. Another alternative is to prevent viral proteins from interacting with membrane cholesterol. At least some of the drugs that are currently tested – for example, polyphenolic substances like quercetin and saponin glycyrrhizin [119, 120] – can act at the protein/cholesterol interface and hinder cholesterol binding by the CRAC motif of the viral S protein and thus inhibit the assembly of new viral particles. Glycyrrhizin, an active component of liquorice roots, was shown to inhibit SARS-CV replication in Vero cells and replication of SARS-associated coronavirus [121, 122]. However, such agents are not very selective and can affect other cholesterol-dependent proteins and therefore cause side effects. Perhaps specially designed CRAC-peptides specifically blocking the interactions of S-protein with cholesterol will prevent the cellular cholesterol loss leading to permeabilization of membranes, oxidative stress, and cell death. The ability of CRAC-containing peptides to regulate cholesterol-dependent cell functions has been demonstrated in a number of works [17, 109, 122, 123], and studies

of the antiviral activity of these peptides may be useful and promising.

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

The work was partially supported by the Russian Foundation for Basic Research

The author declares that there is no conflict of interest.

**68**

Antonina Dunina-Barkovskaya Belozersky Institute of Physico-Chemical Biology, Moscow Lomonosov State University, Moscow, Russia

\*Address all correspondence to: dunina@belozersky.msu.ru

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