SARS-CoV-2 hijacks body's metabolism to amplify COVID-19 severity Metabolism SARSCoV2 Coronavirus Disease COVID SciReports
Study: Metabolic alterations upon SARS-CoV-2 infection and potential therapeutic targets against coronavirus infection. Image Credit: NIAID
Studies have shown that viruses can alter host lipid metabolism to create replication compartments. In COVID-19 patients, an accumulation of lipids has been observed in the lungs. Lipid pattern alterations induced by SARS-CoV-2 have been found to associate with disease severity. Lipid rafts are microdomains containing lipid molecules, including cholesterols and sphingolipids. Evidence shows that lipid rafts located at the host cell membrane play crucial roles in the SARS-CoV-2 entry process by providing platforms for membrane receptors. Lipid rafts can also support cell-to-cell viral transmission by facilitating syncytia formation.
Various sphingolipids, especially ceramide, and sphingosine, play prominent roles in SARS-CoV-2 host cell entry. Ceramide is converted from sphingomyelin by acid sphingomyelinase or synthesized de novo from palmitoyl CoA and serine. Ceramide has been found to facilitate SARS-CoV-2 entry by forming ceramide-rich microdomains where ACE2 clusters. Several ASM inhibitors have been found to prevent SARS-CoV-2 entry by altering surface ceremide levels.
In contrast, covalent attachment of fatty acids to the spike protein has been found to promote viral entry by stabilizing the spike protein homotrimer. Spike protein palmitoylation is a conserved process across all coronaviruses. Recent evidence has shown that SARS-CoV-2 utilizes host lipid droplets to meet the energy demand of replication. TMEM41B, an ER-localized protein responsible for lipid mobilization from lipid droplets, has been identified as a vital host factor for SARS-CoV-2 replication.
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