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Zika virus inhibits type-I interferon production and downstream signaling

Kumar, Anil ; Hou, Shangmei ; Airo, Adriana M ; Limonta, Daniel ; Mancinelli, Valeria ; Branton, William ; Power, Christopher ; Hobman, Tom C

EMBO reports, 2016-12, Vol.17 (12), p.1766-1775 [Periódico revisado por pares]

England: Blackwell Publishing Ltd

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  • Título:
    Zika virus inhibits type-I interferon production and downstream signaling
  • Autor: Kumar, Anil ; Hou, Shangmei ; Airo, Adriana M ; Limonta, Daniel ; Mancinelli, Valeria ; Branton, William ; Power, Christopher ; Hobman, Tom C
  • Assuntos: A549 Cells ; Adult ; flavivirus ; HEK293 Cells ; Host-Pathogen Interactions ; Humans ; Interferon ; interferon response ; Interferon Type I - immunology ; Interferon Type I - metabolism ; NS5 ; Pathogenesis ; Protein Binding ; Proteins ; Scientific Report ; Scientific Reports ; Signal Transduction ; STAT2 ; STAT2 Transcription Factor - metabolism ; Viral Nonstructural Proteins - genetics ; Viral Nonstructural Proteins - metabolism ; Zika virus ; Zika Virus - immunology ; Zika Virus - pathogenicity ; Zika Virus Infection - immunology ; Zika Virus Infection - metabolism ; Zika Virus Infection - virology
  • É parte de: EMBO reports, 2016-12, Vol.17 (12), p.1766-1775
  • Notas: Li Ka Shing Institute of Virology
    ark:/67375/WNG-QDGJ7FX1-9
    Canadian Institutes of Health Research (CIHR) - No. MOP-125903
    Alberta Innovates-Health Solutions
    istex:26D61825C5D949870F8A3F80B2AA135CCFBA77D2
    Expanded View Figures PDFTable EV1Table EV2Table EV3Review Process File
    Women & Children's Health Research Institute - No. 1855
    ArticleID:EMBR201642627
    ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
    These authors contributed equally to this work
  • Descrição: Zika virus is an emerging mosquito‐borne pathogen that is associated with Guillain–Barré syndrome in adults and microcephaly and other neurological defects in newborns. Despite being declared an international emergency by the World Health Organization, comparatively little is known about its biology. Here, we investigate the strategies employed by the virus to suppress the host antiviral response. We observe that once established, Zika virus infection is impervious to interferon treatment suggesting that the virus deploys effective countermeasures to host cell defences. This is confirmed by experiments showing that Zika virus infection impairs the induction of type‐I interferon as well as downstream interferon‐stimulated genes. Multiple viral proteins affect these processes. Virus‐mediated degradation of STAT2 acts to reduce type‐I and type‐III interferon‐mediated signaling. Further, the NS5 of Zika virus binds to STAT2, and its expression is correlated with STAT2 degradation by the proteasome. Together, our findings provide key insights into how Zika virus blocks cellular defense systems. This in turn is important for understanding pathogenesis and may aid in designing antiviral therapies. Synopsis Zika virus (ZIKV) is a mosquito‐borne pathogen that causes Guillain–Barré syndrome in adults and microcephaly in newborns. This report shows that ZIKV infection inhibits the induction of type‐I interferons by downregulating IRF3 and antiviral NF‐κB‐mediated signaling and targets STAT2 for proteasomal degradation. ZIKV NS1, NS4A, and NS5 interfere with the induction of type‐I interferon. ZIKV infection inhibits type‐I interferon signaling. ZIKV infection results in depletion of STAT2 in human cells. ZIKV NS5 interacts with STAT2 and induces proteasomal degradation of the protein. Zika virus (ZIKV) is a mosquito‐borne pathogen that causes Guillain–Barré syndrome in adults and microcephaly in newborns. This report shows that ZIKV infection inhibits the induction of type‐I interferons by downregulating IRF3 and antiviral NF‐κB‐mediated signaling and targets STAT2 for proteasomal degradation.
  • Editor: England: Blackwell Publishing Ltd
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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