A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants

Scotland E. Farley, Jennifer E. Kyle, Hans C. Leier, Lisa M. Bramer, Jules B. Weinstein, Timothy A. Bates, Joon-Yong Lee, Thomas O. Metz, Carsten Schultz and Fikadu G. Tafesse ()
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Scotland E. Farley: Oregon Health & Science University
Jennifer E. Kyle: Pacific Northwest National Laboratory (PNNL)
Hans C. Leier: Oregon Health & Science University
Lisa M. Bramer: Pacific Northwest National Laboratory (PNNL)
Jules B. Weinstein: Oregon Health & Science University
Timothy A. Bates: Oregon Health & Science University
Joon-Yong Lee: Pacific Northwest National Laboratory (PNNL)
Thomas O. Metz: Pacific Northwest National Laboratory (PNNL)
Carsten Schultz: Oregon Health & Science University
Fikadu G. Tafesse: Oregon Health & Science University

Nature Communications, 2022, vol. 13, issue 1, 1-14

Abstract: Abstract A comprehensive understanding of host dependency factors for SARS-CoV-2 remains elusive. Here, we map alterations in host lipids following SARS-CoV-2 infection using nontargeted lipidomics. We find that SARS-CoV-2 rewires host lipid metabolism, significantly altering hundreds of lipid species to effectively establish infection. We correlate these changes with viral protein activity by transfecting human cells with each viral protein and performing lipidomics. We find that lipid droplet plasticity is a key feature of infection and that viral propagation can be blocked by small-molecule glycerolipid biosynthesis inhibitors. We find that this inhibition was effective against the main variants of concern (alpha, beta, gamma, and delta), indicating that glycerolipid biosynthesis is a conserved host dependency factor that supports this evolving virus.

Date: 2022
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DOI: 10.1038/s41467-022-31097-7

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