MENU

Inhibition of SARS-CoV-2 Infections in Engineered Human Tissues Using Clinical-Grade Soluble Human ACE2

Monteil, V; Kwon, H; Prado, P; Hagelkruys, A; Wimmer, RA; Stahl, M; Leopoldi, A; Garreta, E; del Pozo, CH; Prosper, F; Romero, JP; Wirnsberger, G; Zhang, H; Slutsky, AS; Conder, R; Montserrat, N; Mirazimi, A; Penninger, JM

CELL
2020
VL / 181 - BP / 905 - EP / +
abstract
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.
91st Global

AccesS level

Green Published, Other Gold

Mentions data

PAPER MENTIONS
Biology & Biochemistry
  •   Twitter
  • 501
  •   Wikipedia
  • 2
  •   News
  • 110
  •   Policy
  • 0
Molecular Biology & Genetics
  •   Twitter
  • 501
  •   Wikipedia
  • 2
  •   News
  • 110
  •   Policy
  • 0
Global Ranking
  •   Twitter
  • 501
  •   Wikipedia
  • 2
  •   News
  • 110
  •   Policy
  • 0

Mentions Chart

Influratio by dimension
  • Twitter
  • Wikipedia
  • News
  • Policy
PAPER MENTIONS
  •   Twitter
  • 501
  •   Wikipedia
  • 2
  •   News
  • 110
  •   Policy
  • 0
PROYECTO FINANCIADO POR PLAN NACIONAL DE INVESTIGACIÓN AGENCIA ESTATAL DE INVESTIGACIÓN, MINISTERIO DE CIENCIA E INNOVACIÓN. PID2019-109127RB-I00