Abstract
The human coronaviruses (CoVs) severe acute respiratory syndrome (SARS)-CoV and NL63 employ angiotensin-converting enzyme 2 (ACE2) for cell entry. It was shown that recombinant SARS-CoV spike protein (SARS-S) downregulates ACE2 expression and thereby promotes lung injury. Whether NL63-S exerts a similar activity is yet unknown. We found that recombinant SARS-S bound to ACE2 and induced ACE2 shedding with higher efficiency than NL63-S. Shedding most likely accounted for the previously observed ACE2 downregulation but was dispensable for viral replication. Finally, SARS-CoV but not NL63 replicated efficiently in ACE2-positive Vero cells and reduced ACE2 expression, indicating robust receptor interference in the context of SARS-CoV but not NL63 infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiotensin-Converting Enzyme 2
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Animals
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Cell Line
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Chlorocebus aethiops
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Coronavirus / metabolism
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Coronavirus / pathogenicity*
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Down-Regulation*
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Humans
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Membrane Glycoproteins / metabolism*
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Peptidyl-Dipeptidase A / genetics
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Peptidyl-Dipeptidase A / metabolism*
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Severe acute respiratory syndrome-related coronavirus / metabolism
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Severe acute respiratory syndrome-related coronavirus / pathogenicity*
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Spike Glycoprotein, Coronavirus
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Transfection
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Vero Cells
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Viral Envelope Proteins / metabolism*
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Virus Replication
Substances
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Membrane Glycoproteins
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Spike Glycoprotein, Coronavirus
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Viral Envelope Proteins
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Peptidyl-Dipeptidase A
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ACE2 protein, human
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Angiotensin-Converting Enzyme 2