ArticleJournal of virology2023
Pseudorabies Virus Infection Activates the TLR-NF-κB Axis and AIM2 Inflammasome To Enhance Inflammatory Responses in Mice.
Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Pseudorabies virus pUL40 drives inflammatory signaling through competitive hijacking of EphA2 from the Akt-EphA2 interaction.Veterinary research · 2026Article
- Clitocine suppresses TNBC progression by boosting CCRL2 to block survival signals and neutrophil-driven inflammation.Journal of biological engineering · 2026Article
- Pseudorabies virus infection induces IRF1-dependent PANoptosis to provoke the excessive release of HMGB1 and IL-1β.Communications biology · 2026Article
- 2'-5' Oligoadenylate Synthetase-Like 1- (OASL1-) deficient mice promote antiviral protection against pseudorabies virus infection associated with enhanced production of type I interferon.Scientific reports · 2026Article
- Rhynchophylline attenuates porcine pseudorabies virus-induced astrocyte injury by modulating oxidative stress, inflammation, and metabolic abnormalities.Frontiers in pharmacology · 2026Article
- Pseudorabies virus gM protein and herpesvirus homologs block selective autophagy to enhance viral replication.Autophagy · 2025Article
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Immuno-metabolic diseases and therapeutics: molecular mechanisms via inflammasome signaling.Cell communication and signaling : CCS · 2025Review
- Pseudorabies virus induces natural killer cell depletion by GSDMD-mediated inflammation and pyroptosis to promote infection and lung injury.Journal of virology · 2025Article
- GSDMD and GSDME exhibit distinct roles in enteric coronavirus PDCoV-induced pyroptosis and inflammatory responses.Journal of virology · 2025Article
- Role of inflammasomes in diabetes mellitus: mechanisms, complications, and therapeutic potential.Molecular biology reports · 2025Review
- Article
- The Association between the NLRP3 Inflammasome and Specific Long-Non Coding RNAs (lncRNAs) in Cancer; New Perspective and Summary of Recent Studies.Cell biochemistry and biophysics · 2025Review
- Alphaherpesvirus in Pets and Livestock.Microorganisms · 2025Review
- FermentedFrontiers in veterinary science · 2025Article
- Therapeutic potential ofFrontiers in veterinary science · 2025Article
- Article
- Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024Review
- Pseudorabies Virus UL4 protein promotes the ASC-dependent inflammasome activation and pyroptosis to exacerbate inflammation.PLoS pathogens · 2024Article
- The Tick Saliva Peptide HIDfsin2 TLR4-Dependently Inhibits the Tick-Borne Severe Fever with Thrombocytopenia Syndrome Virus in Mouse Macrophages.Antibiotics (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudorabies virus (PRV) infection activates inflammatory responses to release robust proinflammatory cytokines, which are critical for controlling viral infection and clearance of PRV. However, the innate sensors and inflammasomes involved in the production and secretion of proinflammatory cytokines during PRV infection remain poorly studied. In this study, we report that the transcription and expression levels of some proinflammatory cytokines, including interleukin 1β (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α), are upregulated in primary peritoneal macrophages and in mice during PRV infection. Mechanistically, Toll-like receptor 2 (TLR2), TLR3, TLR4, and TLR5 were induced by the PRV infection to enhance the transcription levels of pro-IL-1β, pro-IL-18, and gasdermin D (GSDMD). Additionally, we found that PRV infection and transfection of its genomic DNA triggered AIM2 inflammasome activation, apoptosis-related speckle-like protein (ASC) oligomerization, and caspase-1 activation to enhance the secretion of IL-1β and IL-18, which was mainly dependent on GSDMD, but not GSDME,
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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.