ArticlePLoS pathogens2025
PRRSV-2 nsp2 Ignites NLRP3 inflammasome through IKKβ-dependent dispersed trans-Golgi network translocation.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Pathogenicity and virulence of PRRSV: From regulated cell death reprogramming landscape and immune subversion to precision vaccinology.Virulence · 2026Review
- Antiviral Activity of Baicalin Against PRRSV In Vitro and in Infected Piglets.Veterinary sciences · 2026Article
- Infectious bronchitis virus accessory protein 3a induces renal inflammatory injury by activating the NLRP3 inflammasome via ER calcium mobilization and mitochondrial ROS production.Journal of virology · 2026Article
- Diverse Scaffolds Facilitate NLRP3 Clustering and Inflammasome Formation in Response to Perturbations in Cell Homeostasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Sodium Copper Chlorophyllin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection Through Multiple Antiviral Mechanisms.Transboundary and emerging diseases · 2026Article
- The biological functions of PRRSV nonstructural protein NSP2 in viral infection and replication and its role in host regulatory mechanisms.Frontiers in veterinary science · 2026Review
- PRRSV NSP5 orchestrates dual immune disruption by targeting NLRP3 and STING.Veterinary research · 2025Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The NLRP3 inflammasome is a fundamental component of the innate immune system, yet its excessive activation is intricately associated with viral pathogenesis. Porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2), belonging to the family Arteriviridae, triggers dysregulated cytokine release and interstitial pneumonia, which can quickly escalate to acute respiratory distress and death. However, a mechanistic understanding of PRRSV-2 progression remains unclear. Here, we screen that PRRSV-2 nsp2 activates the NLRP3 inflammasome, thereby instigating a state of hyperinflammation. Mechanistically, PRRSV-2 nsp2 interacts with the nucleotide-binding and oligomerization (NACHT) domain of NLRP3, augmenting IKKβ recruitment to driving NLRP3 translocation to the dispersed trans-Golgi network (dTGN) for oligomerization. This process facilitates ASC polymerization, culminating in the activation of the NLRP3 inflammasome. In addition, the IKKβ-dependent NLRP3 translocation to the dTGN is pivotal for pseudorabies virus (PRV) and encephalomyocarditis virus (EMCV)-induced inflammatory responses. Collectively, these results elucidate a novel mechanism of NLRP3 inflammasome activation during PRRSV-2 infection, providing valuable insights into PRRSV-2 pathogenesis.
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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.