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10.3389/fcimb.2021.766922

http://scihub22266oqcxt.onion/10.3389/fcimb.2021.766922
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suck abstract from ncbi


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pmid34950606      Front+Cell+Infect+Microbiol 2021 ; 11 (ä): 766922
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  • Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Membrane (M) and Spike (S) Proteins Antagonize Host Type I Interferon Response #MMPMID34950606
  • Zhang Q; Chen Z; Huang C; Sun J; Xue M; Feng T; Pan W; Wang K; Dai J
  • Front Cell Infect Microbiol 2021[]; 11 (ä): 766922 PMID34950606show ga
  • Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide and has infected more than 250 million people. A typical feature of COVID-19 is the lack of type I interferon (IFN-I)-mediated antiviral immunity in patients. However, the detailed molecular mechanisms by which SARS-CoV-2 evades the IFN-I-mediated antiviral response remain elusive. Here, we performed a comprehensive screening and identified a set of SARS-CoV-2 proteins that antagonize the IFN-I response. Subsequently, we characterized the mechanisms of two viral proteins antagonize IFN-I production and downstream signaling. SARS-CoV-2 membrane protein binds to importin karyopherin subunit alpha-6 (KPNA6) to inhibit interferon regulatory factor 3(IRF3) nuclear translocation. Further, the spike protein interacts with signal transducer and activator of transcription 1 (STAT1) to block its association with Janus kinase 1 (JAK1). This study increases our understanding of SARS-CoV-2 pathogenesis and suggests novel therapeutic targets for the treatment of COVID-19.
  • |*COVID-19[MESH]
  • |*Interferon Type I[MESH]
  • |*Spike Glycoprotein, Coronavirus[MESH]
  • |*Viral Matrix Proteins[MESH]
  • |Humans[MESH]
  • |SARS-CoV-2[MESH]
  • |Signal Transduction[MESH]


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