ArticleCell death & disease2019
RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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78 citing papers in PubMed, 121 citations in OpenAlex.
- Cytokine levels associated with favorable clinical outcome in the CAPSID randomized trial of convalescent plasma in patients with severe COVID-19.Frontiers in immunology · 2022Trial
- Molecular mechanisms of NLR proteins in inflammasome activation.Communications biology · 2026Review
- Antiviral drug discovery and development: challenges and future directions.Signal transduction and targeted therapy · 2026Review
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- Syncytial death mediated by oncolytic rVSV-NDV dynamically activates immunogenic apoptosis and necroptosis in human lung cancer cells.Molecular therapy. Oncology · 2025Article
- The Neglected Role of GSDMD C-Terminal in Counteracting Type I Interferon Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Expression of intron-containing HIV-1 RNA induces NLRP1 inflammasome activation in myeloid cells.PLoS biology · 2025Article
- The EMCV protein 2B* is required for efficient cell lysis via both caspase-3-dependent and -independent pathways during infection.The Journal of general virology · 2025Article
- PRRSV-2 nsp2 Ignites NLRP3 inflammasome through IKKβ-dependent dispersed trans-Golgi network translocation.PLoS pathogens · 2025Article
- Bacillus cereus cereolysin O induces pyroptosis in an undecapeptide-dependent manner.Cell death discovery · 2024Article
- Article
- Molecular crosstalk between circadian clock and NLRP3 inflammasome signaling in Parkinson's disease.Heliyon · 2024Review
- The genetic advantage of healthy centenarians: unraveling the central role of NLRP3 in exceptional healthspan.Frontiers in aging · 2024Review
- Diacerein reduces inflammasome activation and SARS-CoV-2 virus replication: a proof-of-concept translational study.Frontiers in pharmacology · 2024Article
- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
- The NLRP3 inflammasome in viral infection (Review).Molecular medicine reports · 2023Review
- Activation of Inflammasome during Bluetongue Virus Infection.Pathogens (Basel, Switzerland) · 2023Article
- How much (evil) intelligence can be encoded by 30 kb?Biologia futura · 2023Article
- Chalcone: A potential scaffold for NLRP3 inflammasome inhibitors.European journal of medicinal chemistry reports · 2023Article
- Dissecting Platelet's Role in Viral Infection: A Double-Edged Effector of the Immune System.International journal of molecular sciences · 2023Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early detection of viruses by the innate immune system is crucial for host defense. The NLRP3 inflammasome, through activation of caspase-1, promotes the maturation of IL-1β and IL-18, which are critical for antiviral immunity and inflammatory response. However, the mechanism by which viruses activate this inflammasome is still debated. Here, we report that the replication of cytopathogenic RNA viruses such as vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) induced a lytic cell death leading to potassium efflux, the common trigger of NLRP3 inflammasome activation. This lytic cell death was not prevented by a chemical or genetic inhibition of apoptosis, pyroptosis, or necroptosis but required the viral replication. Hence, the viruses that stimulated type I IFNs production after their sensing did not activate NLRP3 inflammasome due to an inhibition of their replication. In contrast, NLRP3 inflammasome activation induced by RNA virus infection was stimulated in IFNAR-deficient or MAVS-deficient cells consequently to an increased viral replication and ensuing lytic cell death. Therefore, in a context of inefficient IFN response, viral replication-induced lytic cell death activates of the NLRP3 inflammasome to fight against infection.
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