ArticleeLife2024
Ebola virus sequesters IRF3 in viral inclusion bodies to evade host antiviral immunity.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular Insights into High-Pathogenicity RNA Viruses.Viruses · 2026Review
- Hiding in Plain Sight: HIV-1 Membraneless Organelles as Nuclear Hubs-Host Hijacking, Replication, Immune Evasion, and Drug-Access Implications.Pathogens (Basel, Switzerland) · 2026Review
- Review
- A sex-biased response of the adult brain to Zika virus infection: from down-regulation of neuronal IRF3 to enhanced pathology in adult female mice.Cell communication and signaling : CCS · 2026Article
- Grass carp reovirus VP35 hijacks DHX15 into phase-separated inclusion bodies to evade host antiviral immunity.Cell communication and signaling : CCS · 2026Article
- Review
- Participation of host cell proteins in inclusion bodies of non-segmented RNA virus infected cells: a molecular insight.Virology journal · 2025Review
- Long-term clinical sequelae among Sudan ebolavirus disease survivors 2 years post-infection: a matched cohort study.BMC medicine · 2025Article
- Grass carp Trim47 restricts GCRV infection via SPRY domain-mediated autophagic degradation of nonstructural proteins and disruption of viral inclusion bodies.Frontiers in immunology · 2025Article
- Genomic transfers help to decipher the ancient evolution of filoviruses and interactions with vertebrate hosts.PLoS pathogens · 2024Article
- Negative and ambisense RNA virus ribonucleocapsids: more than protective armor.Microbiology and molecular biology reviews : MMBR · 2023Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
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(I:C) 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.