期刊
JOURNAL OF VIROLOGY
卷 84, 期 2, 页码 1198-1205出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01248-09
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资金
- BMBF [01 KI 0705, 01KI 0703]
- Center for Infection Biology
- Hannover Medical School
- National Institute of Allergy and Infectious Diseases [R01AI074986]
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 down-regulation 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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