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10.1016/j.virusres.2019.197843

http://scihub22266oqcxt.onion/10.1016/j.virusres.2019.197843
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31884203!7114844!31884203
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suck abstract from ncbi


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pmid31884203      Virus+Res 2020 ; 278 (ä): 197843
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  • Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-beta production via blocking IPS-1 and RIG-I #MMPMID31884203
  • Zhou Z; Sun Y; Yan X; Tang X; Li Q; Tan Y; Lan T; Ma J
  • Virus Res 2020[Mar]; 278 (ä): 197843 PMID31884203show ga
  • Swine acute diarrhea syndrome coronavirus (SADS-CoV), a newly emerging enteric coronavirus, is considered to be associated with swine acute diarrhea syndrome (SADS) which has caused significantly economic losses to the porcine industry. Interactions between SADS-CoV and the host innate immune response is unclear yet. In this study, we used IPEC-J2 cells as a model to explore potential evasion strategies employed by SADS-CoV. Our results showed that SADS-CoV infection failed to induce IFN-beta production, and inhibited poly (I:C) and Sendai virus (SeV)-triggered IFN-beta expression. SADS-CoV also blocked poly (I:C)-induced phosphorylation and nuclear translocation of IRF-3 and NF-kappaB. Furthermore, SADS-CoV did not interfere with the activity of IFN-beta promoter stimulated by IRF3, TBK1 and IKKepsilon, but counteracted its activation induced by IPS-1 and RIG-I. Collectively, this study is the first investigation that shows interactions between SADS-CoV and the host innate immunity, which provides information of the molecular mechanisms underlying SASD-CoV infection.
  • |Active Transport, Cell Nucleus[MESH]
  • |Alphacoronavirus/*physiology[MESH]
  • |Animals[MESH]
  • |Cell Line[MESH]
  • |Cell Nucleus/metabolism[MESH]
  • |Coronavirus Infections/*immunology/virology[MESH]
  • |DEAD Box Protein 58/*antagonists & inhibitors/metabolism[MESH]
  • |Host-Pathogen Interactions/immunology[MESH]
  • |Immunity, Innate[MESH]
  • |Interferon Regulatory Factor-3/metabolism[MESH]
  • |Interferon-beta/*antagonists & inhibitors/genetics/metabolism[MESH]
  • |NF-kappa B/metabolism[MESH]
  • |Phosphorylation[MESH]
  • |Promoter Regions, Genetic[MESH]
  • |Signal Transduction[MESH]


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