ArticleJournal of virology2021
Pseudorabies Virus Infection Triggers NF-κB Activation via the DNA Damage Response but Actively Inhibits NF-κB-Dependent Gene Expression.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- ERK-METTL3 axis acts as a novel regulator of antiviral innate immunity combating pseudorabies virus infection.PLoS pathogens · 2025Article
- PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue.Microorganisms · 2025Article
- Seneca Valley virus infection exploits DNA damage response to facilitate viral replication.Journal of virology · 2025Article
- BEV 2C protein inhibits the NF-κB signalling pathway to promote viral replication by targeting IKBKB and p65.Veterinary research · 2025Article
- Article
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
- Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024Review
- Article
- HIV-1 Vpr-induced DNA damage activates NF-κB through ATM-NEMO independent of cell cycle arrest.bioRxiv : the preprint server for biology · 2024Article
- Apoptosis is mediated by FeHV-1 through the intrinsic pathway and interacts with the autophagic process.Virology journal · 2023Article
- Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.Viruses · 2023Review
- Several Alphaherpesviruses Interact Similarly with the NF-κB Pathway and Suppress NF-κB-Dependent Gene Expression.Microbiology spectrum · 2023Article
- Pseudorabies Virus Infection Activates the TLR-NF-κB Axis and AIM2 Inflammasome To Enhance Inflammatory Responses in Mice.Journal of virology · 2023Article
- Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis.Veterinary sciences · 2023Article
- Pseudorabies virus exploits NFrontiers in microbiology · 2023Article
- Coinfection of Porcine Circovirus 2 and Pseudorabies Virus Enhances Immunosuppression and Inflammation through NF-κB, JAK/STAT, MAPK, and NLRP3 Pathways.International journal of molecular sciences · 2022Article
- Peptidomic Analysis on Mouse Lung Tissue Reveals AGDP as a Potential Bioactive Peptide against Pseudorabies Virus Infection.International journal of molecular sciences · 2022Article
- Review
- Insights into the Anti-inflammatory and Antiviral Mechanisms of Resveratrol.Mediators of inflammation · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear factor kappa B (NF-κB) pathway is known to integrate signaling associated with very diverse intra- and extracellular stressors, including virus infections, and triggers a powerful (proinflammatory) response through the expression of NF-κB-regulated genes. Typically, the NF-κB pathway collects and transduces threatening signals at the cell surface or in the cytoplasm leading to nuclear import of activated NF-κB transcription factors. In the current work, we demonstrate that the swine alphaherpesvirus pseudorabies virus (PRV) induces a peculiar mode of NF-κB activation known as "inside-out" NF-κB activation. We show that PRV triggers the DNA damage response (DDR) and that this DDR response drives NF-κB activation since inhibition of the nuclear ataxia telangiectasia-mutated (ATM) kinase, a chief controller of DDR, abolished PRV-induced NF-κB activation. Initiation of the DDR-NF-κB signaling axis requires viral protein synthesis but occurs before active viral genome replication. In addition, the initiation of the DDR-NF-κB signaling axis is followed by a virus-induced complete shutoff of NF-κB-dependent gene expression that depends on viral DNA replication. In summary, the results presented in this study reveal that PRV infection triggers a noncanonical DDR-NF-κB activation signaling axis and that the virus actively inhibits the (potentially antiviral) consequences of this pathway, by inhibiting NF-κB-dependent gene expression.
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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 OpenQuestion graph.