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Lack of evidence of ACE2 expression and replicative infection by SARS-CoV-2 in human endothelial cells

Publication

Date: 2nd December 2020 | Source: BioRxiv

Authors: Ian McCracken, Gaye Saginc, Liqun He, Alik Huseynov, Alison Daniels, Sarah Fletcher, Claire Peghaire, Viktoria Kalna, Maarja Andaloussi-Mäe, Lars Muhl, Nicky M. Craig, Samantha J. Griffiths, Jürgen G. Haas, Christine Tait-Burkard, Urban Lendahl, , Graeme M. Birdsey, Christer Betsholtz, Michela Noseda, Andrew Baker, Anna M. Randi.

A striking feature of severe COVID-19 is thrombosis in large as well as small vessels of multiple organs. This has led to the assumption that SARS-CoV-2 virus directly infects and damages the vascular endothelium. However, endothelial expression of ACE2, the cellular receptor for SARS-CoV-2, has not been convincingly demonstrated.

Interrogating human bulk and single-cell transcriptomic data, we found ACE2 expression in endothelial cells to be extremely low or absent in vivo and not upregulated by exposure to inflammatory agents in vitro. Also, the endothelial chromatin landscape at the ACE2 locus showed presence of repressive and absence of activation marks, suggesting that the gene is inactive in endothelial cells. Finally, we failed to achieve infection and replication of SARS-CoV-2 in cultured human endothelial cells, which were permissive to productive infection by coronavirus 229E that uses CD13 as the receptor.

Our data suggest that SARS-Cov-2 is unlikely to infect endothelial cells directly; these findings are consistent with a scenario where endothelial injury is indirectly caused by the infection of neighbouring epithelial cells and/or due to systemic effects mediated by immune cells, platelets, complement activation, and/or proinflammatory cytokines.

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