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SARS-CoV-2 proteins

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    Resistance of endothelial cells to SARS-CoV-2 infection MESHD in vitro

    Authors: Blerina Ahmetaj-Shala; Thomas P Peacock; Laury Baillon; Olivia Swann; Hime Gashaw; Wendy S Barclay; Jane A. Mitchell; Chiara Piubelli; Greta Bergamaschi; Marcella Chiari; Alessandro Gori; Marina Cretich

    doi:10.1101/2020.11.08.372581 Date: 2020-11-09 Source: bioRxiv

    Rationale: The secondary thrombotic MESHD/vascular clinical syndrome of COVID-19 MESHD suggests that SARS-CoV-2 infects MESHD not only respiratory epithelium but also the endothelium activating thrombotic MESHD pathways, disrupting barrier function and allowing access of the virus to other organs of the body. However, a direct test of susceptibility to SARS-CoV-2 of authentic endothelial cell lines has not been performed. Objective: To determine infectibility of primary endothelial cell lines with live SARS-CoV-2 and pseudoviruses expressing SARS-CoV-2 spike PROTEIN protein. Methods and Results: Expression of ACE2 HGNC and BSG pathways genes was determined in three types of endothelial cells; blood outgrowth, lung microvascular and aortic endothelial cells. For comparison nasal epithelial cells, Vero E6 cells (primate kidney fibroblast cell line) and HEK 293T cells (human embryonic kidney cells) transfected with either ACE2 HGNC or BSG were used as controls. Endothelial and Vero E6 cells were treated with live SARS-CoV-2 virus for 1 hour and imaged at 24 and 72 hours post infection. Pseudoviruses containing SARS-CoV-2, Ebola and Vesicular Stomatis Virus MESHD glycoproteins were generated and added to endothelial cells and HEK 239Ts for 2 hours and infection measured using luminescence at 48 hours post infection. Compared to nasal epithelial cells, endothelial cells expressed low or undetectable levels of ACE2 HGNC and TMPRSS2 HGNC but comparable levels of BSG, PPIA HGNC and PPIB HGNC. Endothelial cells showed no susceptibility to live SARS-CoV-2 or SARS-CoV-2 pseudovirus (but showed susceptibility to Ebola and Vesicular Stomatitis Virus MESHD). Overexpression of ACE2 HGNC but not BSG in HEK 239T cells conferred SARS-CoV-2 pseudovirus entry. Endothelial cells primed with IL-1b HGNC remained resistant to SARS-CoV-2. Conclusion: Endothelial cells are resistant to infection with SARS-CoV-2 virus MESHD, in line with relatively low levels of ACE2 HGNC and TMPRSS2 HGNC, suggesting that the vascular dysfunction MESHD and thrombosis MESHD seen in severe COVID-19 MESHD is a result of factors released by adjacent infected cells (e.g. epithelial cells) and/or circulating, systemic inflammatory mediators.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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