Graphical AbstractHighlights d SARS-CoV-2 uses the SARS-CoV receptor ACE2 for host cell entry d The spike protein of SARS-CoV-2 is primed by TMPRSS2 d Antibodies against SARS-CoV spike may offer some protection against SARS-CoV-2

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Highlights d B.1.1.7, B.1.351, and P.1 do not show augmented host cell entry d Entry inhibitors under clinical evaluation block all variants d B.1.351 and P.1 can escape from therapeutic antibodies d B.1.351 and P.1 evade antibodies induced by infection and vaccination

The emergence of a novel, highly pathogenic coronavirus, 2019-nCoV, in China, 24 and its rapid national and international spread pose a global health emergency. 25Coronaviruses use their spike proteins to select and enter target cells and insights into 26 nCoV-2019 spike (S)-driven entry might facilitate assessment of pandemic potential and 27 reveal therapeutic targets. Here, we demonstrate that 2019-nCoV-S uses the SARS-28 coronavirus receptor, ACE2, for entry and the cellular protease TMPRSS2 for 2019-nCoV-29 S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. 30 Finally, we show that the serum form a convalescent SARS patient neutralized 2019-nCoV-31 S-driven entry. Our results reveal important commonalities between 2019-nCoV and 32 SARS-coronavirus infection, which might translate into similar transmissibility and disease 33 pathogenesis. Moreover, they identify a target for antiviral intervention.34 35 One sentence summary: The novel 2019 coronavirus and the SARS-coronavirus share central 36 biological properties which can guide risk assessment and intervention. 37 38 39 40 41 42 43 44 45 46 author/funder. All rights reserved. No reuse allowed without permission.