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Abstract
The pro-homeostatic lipid mediators elovanoids (ELVs) attenuate cell binding and entrance of the SARS-CoV-2 receptor-binding domain (RBD) as well as of the SARS-CoV-2 virus in human primary alveoli cells in culture. We uncovered that very-long-chain polyunsaturated fatty acid precursors (VLC-PUFA, n-3) activate ELV biosynthesis in lung cells. Both ELVs and their precursors reduce the binding to RBD. ELVs downregulate angiotensin-converting enzyme 2 (ACE2) and enhance the expression of a set of protective proteins hindering cell surface virus binding and upregulating defensive proteins against lung damage. In addition, ELVs and their precursors decreased the signal of spike (S) protein found in SARS-CoV-2 infected cells, suggesting that the lipids curb viral infection. These findings open avenues for potential preventive and disease-modifiable therapeutic approaches for COVID-19.
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1 Louisiana State University Health New Orleans, Neuroscience Center of Excellence, School of Medicine, New Orleans, USA (GRID:grid.279863.1) (ISNI:0000 0000 8954 1233)
2 Tulane National Primate Research Center, Covington, USA (GRID:grid.265219.b) (ISNI:0000 0001 2217 8588); Tulane University School of Medicine, Department of Microbiology and Immunology, New Orleans, USA (GRID:grid.265219.b) (ISNI:0000 0001 2217 8588)
3 University of Southern California, Department of Chemistry and Loker Hydrocarbon Research Institute, Los Angeles, USA (GRID:grid.42505.36) (ISNI:0000 0001 2156 6853)