新冠病毒进入细胞依赖于ACE2和TMPRSS2
2020-03-06   阅读:444   来源:细胞

近日,德国哥廷根大学Stefan Pöhlmann、Markus Hoffmann等研究人员合作发现,新冠病毒(SARS-CoV-2)进入细胞依赖ACE2和TMPRSS2,并能够被临床验证的蛋白酶抑制剂所阻断。2020年3月6日,国际知名学术期刊《细胞》在线发表了这一成果。

研究人员证明了新冠病毒使用SARS-CoV受体ACE2进入细胞,并且丝氨酸蛋白酶TMPRSS2用于突刺(S)蛋白的活化。批准用于临床的TMPRSS2抑制剂可阻止其进入,可能成为治疗方法。

最后,研究人员发现,来自恢复期SARS患者的血清能够交叉中和SARS-2-S引起的进入。这些结果揭示了新冠病毒和SARS-CoV感染之间的重要共性,并确定了抗病毒干预的潜在靶标。

研究人员介绍,冠状病毒进入细胞依赖于病毒刺突蛋白与细胞受体的结合,以及宿主细胞蛋白酶活化的S蛋白。阐明新冠病毒使用哪些细胞分子来进入,可能会为病毒的传播提供见解并揭示治疗靶标。

附:英文原文

Title: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

Author: Markus Hoffmann, Hannah Kleine-Weber, Simon Schroeder, Nadine Krüger, Tanja Herrler, Sandra Erichsen, Tobias S. Schiergens, Georg Herrler, Nai-Huei Wu, Andreas Nitsche, Marcel A. Müller, Christian Drosten, Stefan Phlmann

Issue&Volume: 2020-03-05

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.

DOI: 10.1016/j.cell.2020.02.052

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