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10.1016/j.cell.2020.04.004

http://scihub22266oqcxt.onion/10.1016/j.cell.2020.04.004
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32333836!7181998!32333836
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suck abstract from ncbi


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pmid32333836      Cell 2020 ; 181 (4): 905-913.e7
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  • Inhibition of SARS-CoV-2 Infections in Engineered Human Tissues Using Clinical-Grade Soluble Human ACE2 #MMPMID32333836
  • Monteil V; Kwon H; Prado P; Hagelkruys A; Wimmer RA; Stahl M; Leopoldi A; Garreta E; Hurtado Del Pozo C; Prosper F; Romero JP; Wirnsberger G; Zhang H; Slutsky AS; Conder R; Montserrat N; Mirazimi A; Penninger JM
  • Cell 2020[May]; 181 (4): 905-913.e7 PMID32333836show ga
  • 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.
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Animals[MESH]
  • |Betacoronavirus/*drug effects/genetics/isolation & purification/ultrastructure[MESH]
  • |Blood Vessels/virology[MESH]
  • |COVID-19[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Coronavirus Infections/*drug therapy[MESH]
  • |Humans[MESH]
  • |Kidney/cytology/virology[MESH]
  • |Mice[MESH]
  • |Organoids/virology[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/genetics/metabolism/*pharmacology[MESH]
  • |Pneumonia, Viral/*drug therapy[MESH]
  • |Receptors, Virus/metabolism[MESH]
  • |Recombinant Proteins/*pharmacology[MESH]
  • |SARS-CoV-2[MESH]
  • |Spike Glycoprotein, Coronavirus/metabolism[MESH]


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