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10.1016/j.virol.2021.03.015

http://scihub22266oqcxt.onion/10.1016/j.virol.2021.03.015
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33813212!ä!33813212

suck abstract from ncbi


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pmid33813212      Virology 2021 ; 559 (ä): 46-56
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  • Porcine deltacoronavirus nsp10 antagonizes interferon-beta production independently of its zinc finger domains #MMPMID33813212
  • Fang P; Hong Y; Xia S; Zhang J; Ren J; Zhou Y; Fang L; Xiao S
  • Virology 2021[Jul]; 559 (ä): 46-56 PMID33813212show ga
  • Porcine deltacoronavirus (PDCoV) is a novel swine enteropathogenic coronavirus that causes serious vomiting and diarrhea in piglets. Previous work demonstrated that PDCoV infection inhibits type I interferon (IFN) production. Here, we found that ectopic expression of PDCoV nsp10 significantly inhibited Sendai virus (SeV)-induced IFN-beta production by impairing the phosphorylation and nuclear translocation of two transcription factors, IRF3 and NF-kappaB p65 subunit. Interestingly, experiments with truncated mutants and site-directed mutagenesis revealed that PDCoV nsp10 mutants with missing or destroyed zinc fingers (ZFs) domains also impeded SeV-induced IFN-beta production, suggesting that nsp10 does not require its ZF domains to antagonize IFN-beta production. Further work found that co-expression of nsp10 with nsp14 or nsp16, two replicative enzymes, significantly enhanced the inhibitory effects of nsp10 on IFN-beta. Taken together, our results demonstrate that PDCoV nsp10 antagonizes IFN via a ZF-independent mechanism and has a synergistic effect with nsp14 and nsp16 on inhibiting IFN-beta production.
  • |Animals[MESH]
  • |Cell Line[MESH]
  • |Deltacoronavirus/*metabolism[MESH]
  • |Host-Pathogen Interactions[MESH]
  • |Humans[MESH]
  • |Interferon Regulatory Factor-3/metabolism[MESH]
  • |Interferon-beta/*antagonists & inhibitors/metabolism[MESH]
  • |Mutation[MESH]
  • |Sendai virus/metabolism[MESH]
  • |Signal Transduction[MESH]
  • |Swine[MESH]
  • |Transcription Factor RelA/metabolism[MESH]
  • |Viral Nonstructural Proteins/chemistry/genetics/*metabolism[MESH]


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