JOURNAL ARTICLE

Differential downregulation of ACE2 by the spike proteins of severe acute respiratory syndrome coronavirus and human coronavirus NL63

Ilona Glowacka, Stephanie Bertram, Petra Herzog, Susanne Pfefferle, Imke Steffen, Marcus O Muench, Graham Simmons, Heike Hofmann, Thomas Kuri, Friedemann Weber, Jutta Eichler, Christian Drosten, Stefan Pöhlmann
Journal of Virology 2010, 84 (2): 1198-205
19864379
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.

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