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

Autor: Farley SE; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA.; Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR, USA., Kyle JE; Biological Sciences Division, Earth and Biological Sciences Directorate, Pacific Northwest National Laboratory (PNNL), Richland, WA, USA., Leier HC; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA., Bramer LM; Biological Sciences Division, Earth and Biological Sciences Directorate, Pacific Northwest National Laboratory (PNNL), Richland, WA, USA., Weinstein JB; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA., Bates TA; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA., Lee JY; Biological Sciences Division, Earth and Biological Sciences Directorate, Pacific Northwest National Laboratory (PNNL), Richland, WA, USA., Metz TO; Biological Sciences Division, Earth and Biological Sciences Directorate, Pacific Northwest National Laboratory (PNNL), Richland, WA, USA., Schultz C; Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR, USA., Tafesse FG; Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA. tafesse@ohsu.edu.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2022 Jun 17; Vol. 13 (1), pp. 3487. Date of Electronic Publication: 2022 Jun 17.
DOI: 10.1038/s41467-022-31097-7
Abstrakt: 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.
(© 2022. The Author(s).)
Databáze: MEDLINE
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