SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor.
Cell
; 181(2): 271-280.e8, 2020 04 16.
Article
in English
| MEDLINE | ID: covidwho-4561
ABSTRACT
The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Protease Inhibitors
/
Serine Endopeptidases
/
Coronavirus Infections
/
Peptidyl-Dipeptidase A
/
Virus Internalization
/
Spike Glycoprotein, Coronavirus
/
Betacoronavirus
Type of study:
Prognostic study
/
Randomized controlled trials
Language:
English
Journal:
Cell
Year:
2020
Document Type:
Article
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