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10.11817/j.issn.1672-7347.2020.200299

http://scihub22266oqcxt.onion/10.11817/j.issn.1672-7347.2020.200299
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32879112!ä!32879112

suck abstract from ncbi

pmid32879112      Zhong+Nan+Da+Xue+Xue+Bao+Yi+Xue+Ban 2020 ; 45 (5): 591-597
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  • ?????????????2??????? #MMPMID32879112
  • Wu T; Zhang H; Hu E; Ma J
  • Zhong Nan Da Xue Xue Bao Yi Xue Ban 2020[May]; 45 (5): 591-597 PMID32879112show ga
  • The emergence of novel coronavirus pneumonia which was named as coronavirus disease 2019 (COVID-19) by the World Health Organization, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has posed a serious threat to public health. Notably, COVID-19 has rapidly spread around the world and large amount of people have been infected. There is imminent need to investigate the pathogenesis of SARS-CoV-2 and develop effective therapeutic strategies to contain the epidemic. The spike (S) protein of SARS-CoV-2 mediates viral entry into target cells, with S1 subunit binding to a cellular receptor and S2 subunit fusing viral and host membranes. Angiotensin-converting enzyme 2 (ACE2), previously known as a cell receptor of severe acute respiratory syndrome coronavirus (SARS-CoV), is putatively responsible for mediating COVID-19. In this review, we detail our current understanding of the interaction between S protein and ACE2 in the process of virus infection and the potential pathogenesis of SARS-CoV-2, which has critical implications for exploring the potential therapeutic strategies for COVID-19.
  • |*Coronavirus Infections[MESH]
  • |*Pandemics[MESH]
  • |*Peptidyl-Dipeptidase A[MESH]
  • |*Pneumonia, Viral[MESH]
  • |*Spike Glycoprotein, Coronavirus[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Betacoronavirus/*pathogenicity[MESH]
  • |COVID-19[MESH]
  • |Humans[MESH]
  • |SARS-CoV-2[MESH]


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