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
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't
MeSH terms
- Angiotensin-Converting Enzyme 2
- Animals
- Cell Line
- Chlorocebus aethiops
- Coronavirus / metabolism
- Coronavirus / pathogenicity*
- Down-Regulation*
- Humans
- Membrane Glycoproteins / metabolism*
- Peptidyl-Dipeptidase A / genetics
- Peptidyl-Dipeptidase A / metabolism*
- Severe acute respiratory syndrome-related coronavirus / metabolism
- Severe acute respiratory syndrome-related coronavirus / pathogenicity*
- Spike Glycoprotein, Coronavirus
- Transfection
- Vero Cells
- Viral Envelope Proteins / metabolism*
- Virus Replication
Substances
- Membrane Glycoproteins
- Spike Glycoprotein, Coronavirus
- Viral Envelope Proteins
- Peptidyl-Dipeptidase A
- ACE2 protein, human
- Angiotensin-Converting Enzyme 2