Detalle Publicación

Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2
Autores: Monteil, V.; Kwon, H.; Prado, P.; Hagelkruys, A. ; Wimmer, R. A.; Stahl, M. ; Leopoldi, A.; Garreta, E.; Hurtado del Pozo, C.; Prosper Cardoso, Felipe; Romero Riojas, Juan Pablo; Wirnsberger, G.; Zhang, H.; Slutsky, A. S.; Conder, R.; Montserrat, N.; Mirazimi, A. (Autor de correspondencia); Penninger, J. M.
Título de la revista: CELL
ISSN: 0092-8674
Volumen: 181
Número: 4
Páginas: 905 - 913.e7
Fecha de publicación: 2020
Lugar: WOS
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.