AI Article Synopsis
- Investigated how SARS-CoV-2 affects host lipid metabolism, finding significant changes in 409 lipid species post-infection.
- Demonstrated that lipid droplet flexibility plays a crucial role in the infection process.
- Identified that small-molecule inhibitors targeting glycerolipid biosynthesis can halt viral propagation across major variants, suggesting a common host dependency factor.
Article Abstract
A comprehensive understanding of host dependency factors for SARS-CoV-2 remains elusive. We mapped alterations in host lipids following SARS-CoV-2 infection using nontargeted lipidomics. We found that SARS-CoV-2 rewires host lipid metabolism, altering 409 lipid species up to 64-fold relative to controls. We correlated these changes with viral protein activity by transfecting human cells with each viral protein and performing lipidomics. We found that lipid droplet plasticity is a key feature of infection and that viral propagation can be blocked by small-molecule glycerolipid biosynthesis inhibitors. We found 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8863149 | PMC |
| http://dx.doi.org/10.1101/2022.02.14.480430 | DOI Listing |
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