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10.1016/j.vetmic.2020.108918 http://scihub22266oqcxt.onion/10.1016/j.vetmic.2020.108918 33191000!ä!33191000 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33191000&cmd=llinks): Failed to open stream: HTTP request failed! 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Porcine haemagglutinating encephalomyelitis virus deactivates transcription factor IRF3 and limits type I interferon production |pdf=|usr=}}{{33191000}} gab.com Text Porcine haemagglutinating encephalomyelitis virus deactivates transcription factor IRF3 and limits type I interferon production JO: Vet Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=33191000 #FOAvip Porcine haemagglutinating encephalomyelitis virus (PHEV) is a member of coronavirus that causes acute infectious disease and high mortality in piglets. The transcription factor IRF3 is a central regulator of type I interferon (IFN) innate immune signalling. Here, we report that PHEV infection of RAW264.7 cells results in strong suppression of IFN-beta production in the early stage. A comparative analysis of the upstream effector of IFN-beta transcription demonstrated that deactivation of IRF3, but not p65 or ATF-2 proteins, is uniquely attributed to failure of early IFN-beta induction. Moreover, the RIG-I/MDA5/MAVS/TBK1-dependent protective response that regulates the IRF3 pathway is not disrupted by PHEV and works well underlying the deactivated IRF3-mediated IFN-beta inhibition. After challenge with poly(I:C), a synthetic analogue of dsRNA used to stimulate IFN-beta secretion in the TLR-controlled pathway, we show that PHEV and poly(I:C) regulate IFN-beta-induction via two different pathways. Collectively, our findings reveal that deactivation of IRF3 is a specific mechanism that contributes to termination of type I IFN signalling during early infection with PHEV independent of the conserved RIG-I/MAVS/MDA5/TBK1-mediated innate immune response. Twit Text FOAVip Porcine haemagglutinating encephalomyelitis virus deactivates transcription factor IRF3 and limits type I interferon production ????Vet Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=33191000 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33191000 #FOAvip English Wikipedia <ref>{{Cite pmid|33191000}}</ref> Porcine haemagglutinating encephalomyelitis virus deactivates transcription factor IRF3 and limits type I interferon production #MMPMID33191000 Li Z; Yang Y; Lu H; Zhang J; Xu R; Shi J; Lan Y; Guan J; Zhao K; He H; Gao F; He W Vet Microbiol 2021[Jan]; 252 (ä): 108918 PMID33191000show ga Porcine haemagglutinating encephalomyelitis virus (PHEV) is a member of coronavirus that causes acute infectious disease and high mortality in piglets. The transcription factor IRF3 is a central regulator of type I interferon (IFN) innate immune signalling. Here, we report that PHEV infection of RAW264.7 cells results in strong suppression of IFN-beta production in the early stage. A comparative analysis of the upstream effector of IFN-beta transcription demonstrated that deactivation of IRF3, but not p65 or ATF-2 proteins, is uniquely attributed to failure of early IFN-beta induction. Moreover, the RIG-I/MDA5/MAVS/TBK1-dependent protective response that regulates the IRF3 pathway is not disrupted by PHEV and works well underlying the deactivated IRF3-mediated IFN-beta inhibition. After challenge with poly(I:C), a synthetic analogue of dsRNA used to stimulate IFN-beta secretion in the TLR-controlled pathway, we show that PHEV and poly(I:C) regulate IFN-beta-induction via two different pathways. Collectively, our findings reveal that deactivation of IRF3 is a specific mechanism that contributes to termination of type I IFN signalling during early infection with PHEV independent of the conserved RIG-I/MAVS/MDA5/TBK1-mediated innate immune response. |Animals[MESH] |Betacoronavirus 1/genetics/*immunology[MESH] |Coronavirus Infections/immunology/*veterinary/virology[MESH] |Immunity, Innate[MESH] |Interferon Regulatory Factor-3/*genetics/immunology[MESH] |Interferon-beta/*immunology[MESH] |Mice[MESH] |Poly I-C/pharmacology[MESH] |RAW 264.7 Cells[MESH]Porcine haemagglutinating encephalomyelitis virus deactivates transcri(epmc).pdf DeepDyve Pubget Overpricing