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10.1371/journal.pone.0161793

http://scihub22266oqcxt.onion/10.1371/journal.pone.0161793
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suck abstract from ncbi


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pmid27560627
      PLoS+One 2016 ; 11 (8 ): e0161793
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  • Mumps Virus Induces Protein-Kinase-R-Dependent Stress Granules, Partly Suppressing Type III Interferon Production #MMPMID27560627
  • Hashimoto S ; Yamamoto S ; Ogasawara N ; Sato T ; Yamamoto K ; Katoh H ; Kubota T ; Shiraishi T ; Kojima T ; Himi T ; Tsutsumi H ; Yokota S
  • PLoS One 2016[]; 11 (8 ): e0161793 PMID27560627 show ga
  • Stress granules (SGs) are cytoplasmic granular aggregations that are induced by cellular stress, including viral infection. SGs have opposing antiviral and proviral roles, which depend on virus species. The exact function of SGs during viral infection is not fully understood. Here, we showed that mumps virus (MuV) induced SGs depending on activation of protein kinase R (PKR). MuV infection strongly induced interferon (IFN)-?1, 2 and 3, and IFN-? through activation of IFN regulatory factor 3 (IRF3) via retinoic acid inducible gene-I (RIG-I) and the mitochondrial antiviral signaling (MAVS) pathway. MuV-induced IFNs were strongly upregulated in PKR-knockdown cells. MuV-induced SG formation was suppressed by knockdown of PKR and SG marker proteins, Ras-GTPase-activating protein SH3-domain-binding protein 1 and T-cell-restricted intracellular antigen-1, and significantly increased the levels of MuV-induced IFN-?1. However, viral titer was not altered by suppression of SG formation. PKR was required for induction of SGs by MuV infection and regulated type III IFN (IFN-?1) mRNA stability. MuV-induced SGs partly suppressed type III IFN production by MuV; however, the limited suppression was not sufficient to inhibit MuV replication in cell culture. Our results provide insight into the relationship between SGs and IFN production induced by MuV infection.
  • |Animals [MESH]
  • |Blotting, Western [MESH]
  • |Carrier Proteins/genetics [MESH]
  • |Cell Line [MESH]
  • |Chlorocebus aethiops [MESH]
  • |Cytoplasmic Granules/metabolism/*virology [MESH]
  • |DEAD Box Protein 58/metabolism [MESH]
  • |DNA Helicases [MESH]
  • |Gene Expression [MESH]
  • |Host-Pathogen Interactions [MESH]
  • |Humans [MESH]
  • |Interferon Regulatory Factor-3/metabolism [MESH]
  • |Interferons/*biosynthesis/genetics [MESH]
  • |Microscopy, Confocal [MESH]
  • |Mitochondria/metabolism [MESH]
  • |Mumps virus/*physiology [MESH]
  • |Poly(A)-Binding Proteins/genetics [MESH]
  • |Poly-ADP-Ribose Binding Proteins [MESH]
  • |RNA Helicases [MESH]
  • |RNA Interference [MESH]
  • |RNA Recognition Motif Proteins [MESH]
  • |Receptors, Immunologic [MESH]
  • |Reverse Transcriptase Polymerase Chain Reaction [MESH]
  • |Signal Transduction [MESH]
  • |Stress, Physiological/physiology [MESH]
  • |T-Cell Intracellular Antigen-1 [MESH]
  • |Vero Cells [MESH]


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