Mirazimi, A. (Ali)

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    Inhibition of SARS-CoV-2 Infections in Engineered Human Tissues Using Clinical-Grade Soluble Human ACE2
    (2020) Penninger, J.M. (Josef M.); Hagelkrüys, A. (Astrid); Garreta, E. (Elena); Romero, J.P. (Juan Pablo); Montserrat, N. (Nuria); Hurtado-del-Pozo, C. (Carmen); Leopoldi, A. (Alexandra); Wimmer, R.A. (Reiner A.); Stahl, M. (Martin); Conder, R. (Ryan); Wirnsberger, G. (Gerald); Zhang, H. (Haibo); Prosper-Cardoso, F. (Felipe); Kwon, H. (Hyesoo); Monteil, V. (Vanessa); Slutsky, A.S. (Arthur S.); Mirazimi, A. (Ali); Prado, P. (Patricia)
    We 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.