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10.1016/j.cell.2021.02.053

http://scihub22266oqcxt.onion/10.1016/j.cell.2021.02.053
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suck abstract from ncbi


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pmid33713620      Cell 2021 ; 184 (8): 2212-2228.e12
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  • Soluble ACE2-mediated cell entry of SARS-CoV-2 via interaction with proteins related to the renin-angiotensin system #MMPMID33713620
  • Yeung ML; Teng JLL; Jia L; Zhang C; Huang C; Cai JP; Zhou R; Chan KH; Zhao H; Zhu L; Siu KL; Fung SY; Yung S; Chan TM; To KK; Chan JF; Cai Z; Lau SKP; Chen Z; Jin DY; Woo PCY; Yuen KY
  • Cell 2021[Apr]; 184 (8): 2212-2228.e12 PMID33713620show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause acute respiratory disease and multiorgan failure. Finding human host factors that are essential for SARS-CoV-2 infection could facilitate the formulation of treatment strategies. Using a human kidney cell line-HK-2-that is highly susceptible to SARS-CoV-2, we performed a genome-wide RNAi screen and identified virus dependency factors (VDFs), which play regulatory roles in biological pathways linked to clinical manifestations of SARS-CoV-2 infection. We found a role for a secretory form of SARS-CoV-2 receptor, soluble angiotensin converting enzyme 2 (sACE2), in SARS-CoV-2 infection. Further investigation revealed that SARS-CoV-2 exploits receptor-mediated endocytosis through interaction between its spike with sACE2 or sACE2-vasopressin via AT1 or AVPR1B, respectively. Our identification of VDFs and the regulatory effect of sACE2 on SARS-CoV-2 infection shed insight into pathogenesis and cell entry mechanisms of SARS-CoV-2 as well as potential treatment strategies for COVID-19.
  • |*Virus Internalization[MESH]
  • |Angiotensin-Converting Enzyme 2/*immunology[MESH]
  • |COVID-19/immunology/virology[MESH]
  • |Cell Line[MESH]
  • |Host Microbial Interactions/*immunology[MESH]
  • |Humans[MESH]
  • |Protein Binding[MESH]
  • |SARS-CoV-2/*immunology[MESH]
  • |Spike Glycoprotein, Coronavirus/*immunology[MESH]


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