SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor
Journal
Cell
Journal Volume
181
Journal Issue
2
Pages
271-280
Date Issued
2020
Author(s)
Hoffmann, M.
Kleine-Weber, H.
Schroeder, S.
Kr?ger, N.
Herrler, T.
Erichsen, S.
Schiergens, T.S.
Herrler, G.
Nitsche, A.
M?ller, M.A.
Drosten, C.
P?hlmann, S.
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.
SDGs
Type
journal article