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suck abstract from ncbi


10.1038/s41392-021-00604-5

http://scihub22266oqcxt.onion/10.1038/s41392-021-00604-5
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33980808!8113286!33980808
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suck abstract from ncbi

pmid33980808      Signal+Transduct+Target+Ther 2021 ; 6 (1): 189
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  • The interferon-stimulated exosomal hACE2 potently inhibits SARS-CoV-2 replication through competitively blocking the virus entry #MMPMID33980808
  • Zhang J; Huang F; Xia B; Yuan Y; Yu F; Wang G; Chen Q; Wang Q; Li Y; Li R; Song Z; Pan T; Chen J; Lu G; Zhang H
  • Signal Transduct Target Ther 2021[May]; 6 (1): 189 PMID33980808show ga
  • Since the outbreak of coronavirus disease 2019 (COVID-19), it has become a global pandemic. The spike (S) protein of etiologic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) specifically recognizes human angiotensin-converting enzyme 2 (hACE2) as its receptor, which is recently identified as an interferon (IFN)-stimulated gene. Here, we find that hACE2 exists on the surface of exosomes released by different cell types, and the expression of exosomal hACE2 is increased by IFNalpha/beta treatment. In particular, exosomal hACE2 can specifically block the cell entry of SARS-CoV-2, subsequently inhibit the replication of SARS-CoV-2 in vitro and ex vivo. Our findings have indicated that IFN is able to upregulate a viral receptor on the exosomes which competitively block the virus entry, exhibiting a potential antiviral strategy.
  • |Angiotensin-Converting Enzyme 2/genetics/*metabolism[MESH]
  • |Animals[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Exosomes/genetics/*metabolism/virology[MESH]
  • |HEK293 Cells[MESH]
  • |Humans[MESH]
  • |Interferon-alpha/*pharmacology[MESH]
  • |Interferon-beta/*pharmacology[MESH]
  • |Mice[MESH]
  • |Mice, Transgenic[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Vero Cells[MESH]
  • |Virus Internalization/*drug effects[MESH]


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