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. Preprints2020, 2020050359. https://doi.org/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. https://doi.org/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. Preprints2020, 2020050359. https://doi.org/10.20944/preprints202005.0359.v1
APA Style
Acosta Saltos, F., & Acosta Saltos, A.D. (2020). Entry of SARS-CoV2 through the Basal Surface of Alveolar Endothelial Cells – A Proposed Mechanism Mediated by CD147 in COVID-19. Preprints. https://doi.org/10.20944/preprints202005.0359.v1
Chicago/Turabian Style
Acosta Saltos, F. and Alejandro David Acosta Saltos. 2020 "Entry of SARS-CoV2 through the Basal Surface of Alveolar Endothelial Cells – A Proposed Mechanism Mediated by CD147 in COVID-19" Preprints. https://doi.org/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.
Keywords
Covid-19; Endothelial; CD147; SARS-CoV2
Subject
Biology and Life Sciences, Virology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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
Received:
14 March 2022
The commenter has declared there is no conflict of interests.
Comment:
The capacity of CD147 to mediate Cov-2 entry need to be revised after Shilts 2021 and Fenizia 2021 who both failed to observe direct interaction of CD147 with CoV-2 S protein. Those new evidences strongly suggest CD147 doesn't act as an alternative virus receptor.
Commenter: Nina Cardozo
The commenter has declared there is no conflict of interests.
Commenter: Roland Hübner
The commenter has declared there is no conflict of interests.
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
The commenter has declared there is no conflict of interests.