Preprint Hypothesis Version 1 Preserved in Portico This version is not peer-reviewed

Entry of SARS-CoV2 through the Basal Surface of Alveolar Endothelial Cells – A Proposed Mechanism Mediated by CD147 in COVID-19

Version 1 : Received: 21 May 2020 / Approved: 23 May 2020 / Online: 23 May 2020 (05:26:13 CEST)

How to cite: Acosta Saltos, F.; Acosta Saltos, A.D. Entry of SARS-CoV2 through the Basal Surface of Alveolar Endothelial Cells – A Proposed Mechanism Mediated by CD147 in COVID-19. Preprints 2020, 2020050359 (doi: 10.20944/preprints202005.0359.v1). Acosta Saltos, F.; Acosta Saltos, A.D. Entry of SARS-CoV2 through the Basal Surface of Alveolar Endothelial Cells – A Proposed Mechanism Mediated by CD147 in COVID-19. Preprints 2020, 2020050359 (doi: 10.20944/preprints202005.0359.v1).

Abstract

Severe Covid-19 disease is associated with endothelial infection, viraemia, and multi-organ dysfunction. The process through which SARS-CoV2 causes severe disease is yet to be determined. Here, we propose that in severe Covid-19 infection, SARS-CoV2 reaches the host bloodstream by infecting endothelial cells through their basal surface. This occurs, independently of ACE2, through CD147, a putative SARS-CoV2 receptor. The pathway proposed here encourages research on the mechanisms mediating endothelial cell infection in Covid-19.

Subject Areas

Covid-19; Endothelial; CD147; SARS-CoV2

Comments (2)

Comment 1
Received: 23 May 2020
Commenter: Nina Cardozo
The commenter has declared there is no conflict of interests.
Comment: Very interesting approach.
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Comment 2
Received: 27 May 2020
Commenter: Roland Hübner
The commenter has declared there is no conflict of interests.
Comment: I remain skeptical about Varga et al. showing direct evidence of coronavirus in glomerular endothelial cells: their vesicles lack a crown and have a clear interior where the nuclear proteins should be.

Albeit expressed on vessels, glomerular endothelial cells lack ACE2 hampering entry of SARS2 from the bloodstream.

( BTW, ACE2 expression is not sufficient, a protease [TMPSSR2] is needed to enable membrane fusion )

AFAIK scientists have failed to grow any SARS-CoV-2 from the low RNAaemia detected in the bloodstream (Ct > 37 are routinely not reported as 'positives' by clinical laboratories): residual "virus" seems broken down or otherwise neutralized
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