Monteil, VanessaKwon, HyesooPrado, PatriciaHagelkrüys, AstridWimmer, Reiner A.Stahl, MartinLeopoldi, AlexandraGarreta, ElenaHurtado del Pozo, CarmenProsper, FelipeRomero, Juan PabloWirnberger, GeraldZhang, HaiboSlutsky, Artur S.Conder, RyanMontserrat, NúriaMirazimi, AliPenninger, Josef M.2020-06-152021-04-242020-04-24https://hdl.handle.net/2445/165519We have previously provided the first genetic evidence that angiotensin converting enzyme 2 (ACE2) is the critical receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), and ACE2 protects the lung from injury, providing a molecular explanation for the severe lung failure and death due to SARS-CoV infections. ACE2 has now also been identified as a key receptor for SARS-CoV-2 infections, and it has been proposed that inhibiting this interaction might be used in treating patients with COVID-19. However, it is not known whether human recombinant soluble ACE2 (hrsACE2) blocks growth of SARS-CoV-2. Here, we show that clinical grade hrsACE2 reduced SARS-CoV-2 recovery from Vero cells by a factor of 1,000-5,000. An equivalent mouse rsACE2 had no effect. We also show that SARS-CoV-2 can directly infect engineered human blood vessel organoids and human kidney organoids, which can be inhibited by hrsACE2. These data demonstrate that hrsACE2 can significantly block early stages of SARS-CoV-2 infections.9 p.application/pdfengcc-by-nc-nd (c) Elsevier, 2020http://creativecommons.org/licenses/by-nc-nd/3.0/es/CoronavirusSARS-CoV-2TerapèuticaCoronavirusesSARS-CoV-2Therapeuticsinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccess