A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants
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.
Errataetall: |
UpdateIn: Nat Commun. 2022 Jun 17;13(1):3487. - PMID 35715395 |
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Medienart: |
E-Artikel |
Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - year:2022 |
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Enthalten in: |
bioRxiv : the preprint server for biology - (2022) vom: 15. Feb. |
Sprache: |
Englisch |
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Beteiligte Personen: |
Farley, Scotland E [VerfasserIn] |
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Date Revised 01.03.2024 published: Electronic UpdateIn: Nat Commun. 2022 Jun 17;13(1):3487. - PMID 35715395 Citation Status PubMed-not-MEDLINE |
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doi: |
10.1101/2022.02.14.480430 |
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PPN (Katalog-ID): |
NLM337262845 |
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520 | |a 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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700 | 1 | |a Tafesse, Fikadu G |e verfasserin |4 aut | |
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