What is it about?

Viruses interact with host cell factors for attachment and entry into target cells. The spike (S) protein of coronaviruses facilitates host cell entry and which host cell factors are exploited by the S protein for entry might reveal targets for antiviral intervention. Our study shows that the S protein of SARS-CoV-2 like the S protein of SARS-CoV-1 uses angiotensin converting enzyme 2 (ACE2) as entry receptor and the cellular serine protease TMPRSS2 for S protein activation, i.e. cleavage of the S protein which allows the S protein to transit into an active form. Importantly, TMPRSS2-mediated S protein activation can be inhibited by camostat mesylate, a serine protease inhibitor approved for treatment of pancreatitis in Japan. Finally, our study shows that sera from convalescent SARS patients inhibit host cell entry driven by the S protein of SARS-CoV-2, although with moderate efficiency, indicating that an antibody response raised against SARS-CoV-1 might offer some level of protection against SARS-CoV-2.

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Why is it important?

The studies provides important insights into host-cell interactions of SARS-CoV-2 and shows that the clinically-proven serine protease inhibitor camostat mesylate might be suitable for COVID-19 treatment.

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This page is a summary of: The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells, January 2020, Cold Spring Harbor Laboratory Press, DOI: 10.1101/2020.01.31.929042.
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