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10.21203/rs.3.rs-1576788/v1

http://scihub22266oqcxt.onion/10.21203/rs.3.rs-1576788/v1
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35547851!9094105!35547851
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suck abstract from ncbi


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pmid35547851      Res+Sq 2022 ; ä (ä): ä
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  • CNBP restricts SARS-CoV2 by regulating IFN and disrupting RNA-protein condensates #MMPMID35547851
  • Fitzgerald K; Chen Y; Lei X; Jiang Z; Humphries F; Mustone N; Ramos I; Mutetwa T; Fernandez-Sesma A
  • Res Sq 2022[May]; ä (ä): ä PMID35547851show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evades antiviral immunity through the expression of viral proteins that block detection, signaling, interferon (IFN) induction, and IFN-stimulated gene (ISG) expression(1, 2). Weak induction of type I IFNs is associated with a hyperinflammatory response in patients that develop severe COVID-19(3, 4, 5). Here we uncover a role for cellular nucleic acid-binding protein (CNBP) in restricting SARS-CoV-2. Typically, CNBP resides in the cytosol and, in response to RNA sensing pathways, undergoes phosphorylation, nuclear translocation, and IFNbeta enhancer DNA binding to turn on IFNbeta gene transcription. In SARS-CoV-2-infected cells CNBP coordinates IFNbeta gene transcription. In addition, CNBP binds SARS-CoV-2 viral RNA directly. CNBP competes with the nucleocapsid (N) protein and prevents viral RNA and nucleocapsid protein from undergoing liquid-liquid phase separation (LLPS) forming condensates critical for viral replication. Consequently, cells and animals lacking CNBP have higher viral loads and CNBP-deficient mice succumb rapidly to infection. Altogether, these findings identify CNBP as a key antiviral factor for SARS-CoV-2, functioning both as a regulator of antiviral IFN gene expression and a cell intrinsic restriction factor that disrupts LLPS to limit viral replication and spread.
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