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10.3390/v12010043 http://scihub22266oqcxt.onion/10.3390/v12010043 31905881!7019732!31905881     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31905881&cmd=llinks): Failed to open stream: HTTP request failed! 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Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Production by Cleaving NEMO at Multiple Sites |pdf=|usr=}}{{31905881}} gab.com Text Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Production by Cleaving NEMO at Multiple Sites JO: Viruses http://www.kidney.de/pget.php?&tw=1&pmid=31905881 #FOAvip Feline infectious peritonitis (FIP), caused by virulent feline coronavirus, is the leading infectious cause of death in cats. The type I interferon (type I IFN)-mediated immune responses provide host protection from infectious diseases. Several coronaviruses have been reported to evolve diverse strategies to evade host IFN response. However, whether feline infectious peritonitis virus (FIPV) antagonizes the type I IFN signaling remains unclear. In this study, we demonstrated that FIPV strain DF2 infection not only failed to induce interferon-beta (IFN-beta) and interferon-stimulated gene (ISG) production, but also inhibited Sendai virus (SEV) or polyinosinic-polycytidylic acid (poly(I:C))-induced IFN-beta production. Subsequently, we found that one of the non-structural proteins encoded by the FIPV genome, nsp5, interrupted type I IFN signaling in a protease-dependent manner by cleaving the nuclear factor kappaB (NF-kappaB) essential modulator (NEMO) at three sites-glutamine132 (Q132), Q205, and Q231. Further investigation revealed that the cleavage products of NEMO lost the ability to activate the IFN-beta promoter. Mechanistically, the nsp5-mediated NEMO cleavage disrupted the recruitment of the TRAF family member-associated NF-kappaB activator (TANK) to NEMO, which reduced the phosphorylation of interferon regulatory factor 3 (IRF3), leading to the inhibition of type I IFN production. Our research provides new insights into the mechanism for FIPV to counteract host innate immune response. Twit Text FOAVip Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Production by Cleaving NEMO at Multiple Sites ????Viruses http://www.kidney.de/pget.php?&tw=1&pmid=31905881 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31905881 #FOAvip English Wikipedia <ref>{{Cite pmid|31905881}}</ref> Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Production by Cleaving NEMO at Multiple Sites #MMPMID31905881 Chen S; Tian J; Li Z; Kang H; Zhang J; Huang J; Yin H; Hu X; Qu L Viruses 2019[Dec]; 12 (1): ä PMID31905881show ga Feline infectious peritonitis (FIP), caused by virulent feline coronavirus, is the leading infectious cause of death in cats. The type I interferon (type I IFN)-mediated immune responses provide host protection from infectious diseases. Several coronaviruses have been reported to evolve diverse strategies to evade host IFN response. However, whether feline infectious peritonitis virus (FIPV) antagonizes the type I IFN signaling remains unclear. In this study, we demonstrated that FIPV strain DF2 infection not only failed to induce interferon-beta (IFN-beta) and interferon-stimulated gene (ISG) production, but also inhibited Sendai virus (SEV) or polyinosinic-polycytidylic acid (poly(I:C))-induced IFN-beta production. Subsequently, we found that one of the non-structural proteins encoded by the FIPV genome, nsp5, interrupted type I IFN signaling in a protease-dependent manner by cleaving the nuclear factor kappaB (NF-kappaB) essential modulator (NEMO) at three sites-glutamine132 (Q132), Q205, and Q231. Further investigation revealed that the cleavage products of NEMO lost the ability to activate the IFN-beta promoter. Mechanistically, the nsp5-mediated NEMO cleavage disrupted the recruitment of the TRAF family member-associated NF-kappaB activator (TANK) to NEMO, which reduced the phosphorylation of interferon regulatory factor 3 (IRF3), leading to the inhibition of type I IFN production. Our research provides new insights into the mechanism for FIPV to counteract host innate immune response. |Animals[MESH] |Cats[MESH] |Cell Line[MESH] |Coronavirus 3C Proteases[MESH] |Coronavirus Infections/*immunology[MESH] |Coronavirus, Feline/metabolism/*physiology[MESH] |Cysteine Endopeptidases/genetics/*metabolism[MESH] |I-kappa B Kinase/genetics/*metabolism[MESH] |Immune Evasion[MESH] |Immunity, Innate[MESH] |Interferon Regulatory Factor-3[MESH] |Interferon Type I/*antagonists & inhibitors/metabolism[MESH] |Interferon-beta/antagonists & inhibitors/genetics/metabolism[MESH] |Mutation[MESH] |NF-kappa B/metabolism[MESH] |Promoter Regions, Genetic[MESH] |Signal Transduction[MESH]Feline Infectious Peritonitis Virus Nsp5 Inhibits Type I Interferon Pr(epmc).pdf DeepDyve Pubget Overpricing