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Ebola virus sequesters IRF3 in viral inclusion bodies to evade host antiviral immunity.
Zhu, Lin; Jin, Jing; Wang, Tingting; Hu, Yong; Liu, Hainan; Gao, Ting; Dong, Qincai; Jin, Yanwen; Li, Ping; Liu, Zijing; Huang, Yi; Liu, Xuan; Cao, Cheng.
Affiliation
  • Zhu L; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Jin J; Institute of Physical Science and Information Technology, Anhui University, Hefei, China.
  • Wang T; Institute of Physical Science and Information Technology, Anhui University, Hefei, China.
  • Hu Y; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Liu H; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Gao T; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Dong Q; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Jin Y; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Li P; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Liu Z; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Huang Y; Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
  • Liu X; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
  • Cao C; Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.
Elife ; 122024 Jan 29.
Article in En | MEDLINE | ID: mdl-38285487
ABSTRACT
Viral inclusion bodies (IBs) commonly form during the replication of Ebola virus (EBOV) in infected cells, but their role in viral immune evasion has rarely been explored. Here, we found that interferon regulatory factor 3 (IRF3), but not TANK-binding kinase 1 (TBK1) or IκB kinase epsilon (IKKε), was recruited and sequestered in viral IBs when the cells were infected by EBOV transcription- and replication-competent virus-like particles (trVLPs). Nucleoprotein/virion protein 35 (VP35)-induced IBs formation was critical for IRF3 recruitment and sequestration, probably through interaction with STING. Consequently, the association of TBK1 and IRF3, which plays a vital role in type I interferon (IFN-I) induction, was blocked by EBOV trVLPs infection. Additionally, IRF3 phosphorylation and nuclear translocation induced by Sendai virus or poly(IC) stimulation were suppressed by EBOV trVLPs. Furthermore, downregulation of STING significantly attenuated VP35-induced IRF3 accumulation in IBs. Coexpression of the viral proteins by which IB-like structures formed was much more potent in antagonizing IFN-I than expression of the IFN-I antagonist VP35 alone. These results suggested a novel immune evasion mechanism by which EBOV evades host innate immunity.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Interferon Type I / Hemorrhagic Fever, Ebola / Interferon Regulatory Factor-3 / Immune Evasion / Inclusion Bodies, Viral Limits: Humans Language: En Journal: Elife Year: 2024 Type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Interferon Type I / Hemorrhagic Fever, Ebola / Interferon Regulatory Factor-3 / Immune Evasion / Inclusion Bodies, Viral Limits: Humans Language: En Journal: Elife Year: 2024 Type: Article Affiliation country: China