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10.1128/JVI.00327-21

http://scihub22266oqcxt.onion/10.1128/JVI.00327-21
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33963054!8274604!33963054
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suck abstract from ncbi


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pmid33963054      J+Virol 2021 ; 95 (15): e0032721
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  • ILRUN Downregulates ACE2 Expression and Blocks Infection of Human Cells by SARS-CoV-2 #MMPMID33963054
  • Tribolet L; Alexander MR; Brice AM; van Vuren PJ; Rootes CL; Mara K; McDonald M; Bruce KL; Gough TJ; Shi S; Cowled C; Bean AGD; Stewart CR
  • J Virol 2021[Jul]; 95 (15): e0032721 PMID33963054show ga
  • The human protein-coding gene ILRUN (inflammation and lipid regulator with UBA-like and NBR1-like domains; previously C6orf106) was identified as a proviral factor for Hendra virus infection and was recently characterized to function as an inhibitor of type I interferon expression. Here, we have utilized transcriptome sequencing (RNA-seq) to define cellular pathways regulated by ILRUN in the context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of Caco-2 cells. We find that inhibition of ILRUN expression by RNA interference alters transcription profiles of numerous cellular pathways, including upregulation of the SARS-CoV-2 entry receptor ACE2 and several other members of the renin-angiotensin aldosterone system. In addition, transcripts of the SARS-CoV-2 coreceptors TMPRSS2 and CTSL were also upregulated. Inhibition of ILRUN also resulted in increased SARS-CoV-2 replication, while overexpression of ILRUN had the opposite effect, identifying ILRUN as a novel antiviral factor for SARS-CoV-2 replication. This represents, to our knowledge, the first report of ILRUN as a regulator of the renin-angiotensin-aldosterone system (RAAS). IMPORTANCE There is no doubt that the current rapid global spread of COVID-19 has had significant and far-reaching impacts on our health and economy and will continue to do so. Research in emerging infectious diseases, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is growing rapidly, with new breakthroughs in the understanding of host-virus interactions to assist with the development of innovative and exciting therapeutic strategies. Here, we present the first evidence that modulation of the human protein-coding gene ILRUN functions as an antiviral factor for SARS-CoV-2 infection, likely through its newly identified role in regulating the expression of SARS-CoV-2 entry receptors ACE2, TMPRSS2, and CTSL. These data improve our understanding of biological pathways that regulate host factors critical to SARS-CoV-2 infection, contributing to the development of antiviral strategies to deal with the current SARS-CoV-2 pandemic.
  • |*Down-Regulation[MESH]
  • |*Gene Expression Regulation, Enzymologic[MESH]
  • |Angiotensin-Converting Enzyme 2/*biosynthesis/genetics[MESH]
  • |Animals[MESH]
  • |COVID-19/genetics/*metabolism[MESH]
  • |Caco-2 Cells[MESH]
  • |Cathepsin L/biosynthesis/genetics[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Humans[MESH]
  • |Neoplasm Proteins/genetics/*metabolism[MESH]
  • |Renin-Angiotensin System[MESH]
  • |SARS-CoV-2/genetics/*metabolism[MESH]
  • |Serine Endopeptidases/biosynthesis/genetics[MESH]


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