Here, we demonstrate that 2019-nCoV-S uses the SARS-coronavirus receptor, ACE2, for entry and the cellular protease TMPRSS2 for 2019-nCoV-S priming. A TMPRSS2 inhibitor blocked entry and might constitute a treatment option. Finally, we show that the serum form a convalescent SARS patient neutralized 2019-nCoV-S-driven entry. Our results reveal important commonalities between 2019-nCoV and SARS-coronavirus infection, which might translate into similar transmissibility and disease pathogenesis. Moreover, they identify a target for antiviral intervention.
The present study suggests that 2019-nCoV spread might also depend on TMPRSS2 activity and it is noteworthy that the serine protease inhibitor camostat mesylate blocks TMPRSS2 activity (24, 26) and has been approved in Japan for human use, although for an unrelated indication. This compound or related ones should be considered for treatment of 2019-nCoV infected patients.