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10.3390/v13010047

http://scihub22266oqcxt.onion/10.3390/v13010047
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33396605!7823417!33396605
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suck abstract from ncbi


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pmid33396605      Viruses 2020 ; 13 (1): ä
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  • SARS-CoV-2 Nucleocapsid Protein Interacts with RIG-I and Represses RIG-Mediated IFN-beta Production #MMPMID33396605
  • Chen K; Xiao F; Hu D; Ge W; Tian M; Wang W; Pan P; Wu K; Wu J
  • Viruses 2020[Dec]; 13 (1): ä PMID33396605show ga
  • SARS-CoV-2 is highly pathogenic in humans and poses a great threat to public health worldwide. Clinical data shows a disturbed type I interferon (IFN) response during the virus infection. In this study, we discovered that the nucleocapsid (N) protein of SARS-CoV-2 plays an important role in the inhibition of interferon beta (IFN-beta) production. N protein repressed IFN-beta production induced by poly(I:C) or upon Sendai virus (SeV) infection. We noted that N protein also suppressed IFN-beta production, induced by several signaling molecules downstream of the retinoic acid-inducible gene I (RIG-I) pathway, which is the crucial pattern recognition receptor (PRR) responsible for identifying RNA viruses. Moreover, our data demonstrated that N protein interacted with the RIG-I protein through the DExD/H domain, which has ATPase activity and plays an important role in the binding of immunostimulatory RNAs. These results suggested that SARS-CoV-2 N protein suppresses the IFN-beta response through targeting the initial step, potentially the cellular PRR-RNA-recognition step in the innate immune pathway. Therefore, we propose that the SARS-CoV-2 N protein represses IFN-beta production by interfering with RIG-I.
  • |A549 Cells[MESH]
  • |Animals[MESH]
  • |COVID-19/*immunology[MESH]
  • |DEAD Box Protein 58/genetics/*metabolism[MESH]
  • |HEK293 Cells[MESH]
  • |HeLa Cells[MESH]
  • |Host-Pathogen Interactions/immunology[MESH]
  • |Humans[MESH]
  • |Interferon-beta/*metabolism[MESH]
  • |Nucleocapsid Proteins/*metabolism[MESH]
  • |Protein Interaction Domains and Motifs[MESH]
  • |Receptors, Immunologic[MESH]
  • |SARS-CoV-2/*metabolism[MESH]


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