Please use this identifier to cite or link to this item: https://covid-19.conacyt.mx/jspui/handle/1000/825
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, T
Herrler, G
Wu, N
Nitsche, A
Müller, M
Drosten, C
Pöhlmann, S
Acceso Abierto
Atribución-NoComercial-SinDerivadas
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.
Cell
2020
Preimpreso
https://coronavirus.1science.com/item/f2fa24e402b55b31defd7ef1783cd256b4d13326
Inglés
VIRUS RESPIRATORIOS
Appears in Collections:Artículos científicos

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