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Forschungsdatenbank PMU-SQQUID

SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor.
Hoffmann, M; Kleine-Weber, H; Schroeder, S; Krüger, N; Herrler, T; Erichsen, S; Schiergens, TS; Herrler, G; Wu, NH; Nitsche, A; Müller, MA; Drosten, C; Pöhlmann, S;
Cell. 2020; 181(2): 271-280.e8.
Originalarbeiten (Zeitschrift)

PMU-Autor/inn/en

Erichsen Sandra

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.