Por favor, use este identificador para citar o enlazar este ítem:
http://conacyt.repositorioinstitucional.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 | |
| Aparece en las colecciones: | Artículos científicos |
Cargar archivos:
| Fichero | Tamaño | Formato | |
|---|---|---|---|
| 102661.pdf | 5.58 MB | Adobe PDF | Visualizar/Abrir |