ArticleJournal of virology2020
Respiratory Syncytial Virus Sequesters NF-κB Subunit p65 to Cytoplasmic Inclusion Bodies To Inhibit Innate Immune Signaling.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Liquid-liquid phase separation drives immune signaling transduction in cancer: a bibliometric and visualized study from 1992 to 2024.Frontiers in oncology · 2025Pooled it
- Integration of ATAC-seq and RNA-seq analysis identifies host genes related with PRRSV infection.Veterinary research · 2026Article
- Functional minigenome system reveals polymerase features of swine orthopneumovirus.Journal of virology · 2026Article
- In vitro liquid-liquid phase separation induced by respiratory syncytial virus proteins and RNA.Science advances · 2026Article
- Review
- Human NLRP3 inflammasome activation leads to formation of condensate at the microtubule organizing center.Science advances · 2026Article
- Liquid-liquid phase separation in the viral replication cycle: new paradigms and therapeutic opportunities.Archives of virology · 2026Review
- Liquid-liquid phase separation mediated immune evasion of respiratory syncytial virus against oligoadenylate synthetase-RNase L pathway.PLoS pathogens · 2026Article
- ZNRD2 Mediated Nucleoprotein Aggregation Impairs Respiratory Syncytial Virus Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of α2-adrenergic receptors as a therapeutic strategy for immune rejection in post-surgery osteosarcoma recurrence treatment.Journal of orthopaedic translation · 2026Article
- Human respiratory syncytial virus regulates the expression of interferon-stimulated genes through modulation of fibrillarin.Frontiers in cellular and infection microbiology · 2026Article
- Rational design 2.0: transitioning from static structural biology to computational prioritization and iterative vaccine optimization for RSV.Frontiers in immunology · 2026Review
- When defense backfires: inflammatory determinants of RSV-induced disease severity.Future virology · 2026Article
- Participation of host cell proteins in inclusion bodies of non-segmented RNA virus infected cells: a molecular insight.Virology journal · 2025Review
- Membraneless Organelles and Phase Separation in Tumours: Mechanisms and Prospects.Cell proliferation · 2025Review
- Fatal Case of Viral Pneumonia Associated with Metapneumovirus Infection in a Patient with a Burdened Medical History.Microorganisms · 2025Article
- A designer polyQ fusion protein modulates NF-κB signaling by sequestering P65/RelA into aggregates.Scientific reports · 2025Article
- Respiratory syncytial virus (RSV) enhances translation of virus-resembling AU-rich host transcripts.Virology journal · 2025Article
- The MAPK Response to Virus Infection Is Modified by Probenecid.Current issues in molecular biology · 2025Review
- Advances in development of antiviral strategies against respiratory syncytial virus.Acta pharmaceutica Sinica. B · 2025Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Viruses routinely employ strategies to prevent the activation of innate immune signaling in infected cells. Respiratory syncytial virus (RSV) is no exception, as it encodes two accessory proteins (NS1 and NS2) which are well established to block interferon signaling. However, RSV-encoded mechanisms for inhibiting NF-κB signaling are less well characterized. In this study, we identified RSV-mediated antagonism of this pathway, independent of the NS1 and NS2 proteins and indeed distinct from other known viral mechanisms of NF-κB inhibition. In both human and bovine RSV-infected cells, we demonstrated that the p65 subunit of NF-κB is rerouted to perinuclear puncta in the cytoplasm, which are synonymous with viral inclusion bodies (IBs), the site for viral RNA replication. Captured p65 was unable to translocate to the nucleus or transactivate a NF-κB reporter following tumor necrosis factor alpha (TNF-α) stimulation, confirming the immune-antagonistic nature of this sequestration. Subsequently, we used correlative light electron microscopy (CLEM) to colocalize the RSV N protein and p65 within bovine RSV (bRSV) IBs, which are granular, membraneless regions of cytoplasm with liquid organelle-like properties. Additional characterization of bRSV IBs indicated that although they are likely formed by liquid-liquid phase separation (LLPS), they have a differential sensitivity to hypotonic shock proportional to their size. Together, these data identify a novel mechanism for viral antagonism of innate immune signaling which relies on sequestration of the NF-κB subunit p65 to a biomolecular condensate-a mechanism conserved across the
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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 OpenQuestion graph.