Differential Downregulation of ACE2 by the Spike Proteins of Severe Acute Respiratory Syndrome Coronavirus and Human Coronavirus NL63
-
- Ilona Glowacka
- Institute of Virology, Hannover Medical School, 30625 Hannover, Germany
-
- Stephanie Bertram
- Institute of Virology, Hannover Medical School, 30625 Hannover, Germany
-
- Petra Herzog
- Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Str. 74, 20359 Hamburg, Germany
-
- Susanne Pfefferle
- Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Str. 74, 20359 Hamburg, Germany
-
- Imke Steffen
- Institute of Virology, Hannover Medical School, 30625 Hannover, Germany
-
- Marcus O. Muench
- Blood Systems Research Institute and Department of Laboratory Medicine, University of California, San Francisco, California
-
- Graham Simmons
- Blood Systems Research Institute and Department of Laboratory Medicine, University of California, San Francisco, California
-
- Heike Hofmann
- Department of Medical Microbiology and Virology, University of Kiel, 24105 Kiel, Germany
-
- Thomas Kuri
- Department of Virology, University of Freiburg, 79008 Freiburg, Germany
-
- Friedemann Weber
- Department of Virology, University of Freiburg, 79008 Freiburg, Germany
-
- Jutta Eichler
- Department of Medicinal Chemistry, University of Erlangen-Nürnberg, Schuhstrasse 19, 91052 Erlangen, Germany
-
- Christian Drosten
- Institute of Virology, University of Bonn Medical Centre, Sigmund-Freud-St. 25, 53127 Bonn, Germany
-
- Stefan Pöhlmann
- Institute of Virology, Hannover Medical School, 30625 Hannover, Germany
抄録
<jats:title>ABSTRACT</jats:title><jats:p>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.</jats:p>
収録刊行物
-
- Journal of Virology
-
Journal of Virology 84 (2), 1198-1205, 2010-01-15
American Society for Microbiology