The roles of lipids in SARS-CoV-2 viral replication and the host immune response

Abstract

The significant morbidity and mortality associated with severe acute respiratory syndrome coronavirus 2 infection has underscored the need for novel antiviral strategies. Lipids play essential roles in the viral life cycle. The lipid composition of cell membranes can influence viral entry by mediating fusion or affecting receptor conformation. Upon infection, viruses can reprogram cellular metabolism to remodel lipid membranes and fuel the production of new virions. Furthermore, several classes of lipid mediators, including eicosanoids and sphingolipids, can regulate the host immune response to viral infection. Here, we summarize the existing literature on the mechanisms through which these lipid mediators may regulate viral burden in COVID-19. Furthermore, we define the gaps in knowledge and identify the core areas in which lipids offer therapeutic promise for severe acute respiratory syndrome coronavirus 2.

Keywords: COVID-19; SARS-CoV-2; cholesterol; coronavirus; eicosanoids; lipid metabolism; lipidomics; phospholipids; sphingolipids; viral infection.

Fig. 1

Interactions between coronaviruses and host lipids, including receptor binding and fusion, remodeling of endoplasmic reticulum–derived membranes to form replication organelles, and alterations in lipid metabolism to promote viral replication. Created with BioRender.com.