ArticleThe Journal of biological chemistry2017
PB1-F2 Peptide Derived from Avian Influenza A Virus H7N9 Induces Inflammation via Activation of the NLRP3 Inflammasome.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 106 citations in OpenAlex.
- Long noncoding RNA#61 synergizes with viral PA-X to augment pyroptosis and attenuate the virulence of highly pathogenic H5N1 influenza virus in mice.Journal of virology · 2026Article
- Systems-Level Analysis of HPAI H5N1 Infection in Ducks: Integrating Transcriptomic, Proteomic, and Phosphoproteomic Data.International journal of molecular sciences · 2026Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- Avian Influenza Viruses: Global Panzootic, Host Range Expansion and Emerging One-Health Threats.Veterinary sciences · 2026Review
- Decoupling musculoskeletal damage from antiviral control: the NLRP3 inflammasome in arthritogenic alphavirus infection.Frontiers in cellular and infection microbiology · 2026Review
- The LTB4-BLT1 axis attenuates influenza-induced lung inflammation by suppressing NLRP3 activation.Cell death discovery · 2025Article
- Activation and evasion of inflammasomes during viral and microbial infection.Cellular and molecular life sciences : CMLS · 2025Review
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Mechanistic Insights into Influenza A Virus-Induced Cell Death and Emerging Treatment Strategies.Veterinary sciences · 2024Review
- Review
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Comprehensive pan-cancer analysis of mitochondrial outer membrane permeabilisation activity reveals positive immunomodulation and assists in identifying potential therapeutic targets for immunotherapy resistance.Clinical and translational medicine · 2024Article
- Identification of a short sequence motif in the influenza A virus pathogenicity factor PB1-F2 required for inhibition of human NLRP3.Journal of virology · 2024Article
- Gasdermin D promotes influenza virus-induced mortality through neutrophil amplification of inflammation.Nature communications · 2024Article
- Genomic characterization of equine influenza A subtype H3N8 viruses by long read sequencing and functional analyses of the PB1-F2 virulence factor of A/equine/Paris/1/2018.Veterinary research · 2024Article
- Virus versus host: influenza A virus circumvents the immune responses.Frontiers in microbiology · 2024Review
- Aggregated Hendra virus C-protein activates the NLRP3 inflammasome to induce inflammation.Journal of inflammation (London, England) · 2023Article
- Gasdermin D promotes hyperinflammation and immunopathology during severe influenza A virus infection.Cell death & disease · 2023Article
- The NLRP3 inflammasome in viral infection (Review).Molecular medicine reports · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The emergence of avian H7N9 influenza A virus in humans with associated high mortality has highlighted the threat of a potential pandemic. Fatal H7N9 infections are characterized by hyperinflammation and increased cellular infiltrates in the lung. Currently there are limited therapies to address the pathologies associated with H7N9 infection and the virulence factors that contribute to these pathologies. We have found that PB1-F2 derived from H7N9 activates the NLRP3 inflammasome and induces lung inflammation and cellular recruitment that is NLRP3-dependent. We have also shown that H7N9 and A/Puerto Rico/H1N1 (PR8)PB1-F2 peptide treatment induces significant mitochondrial reactive oxygen production, which contributes to NLRP3 activation. Importantly, treatment of cells or mice with the specific NLRP3 inhibitor MCC950 significantly reduces IL-1β maturation, lung cellular recruitment, and cytokine production. Together, these results suggest that PB1-F2 from H7N9 avian influenza A virus may be a major contributory factor to disease pathophysiology and excessive inflammation characteristic of clinical infections and that targeting the NLRP3 inflammasome may be an effective means to reduce the inflammatory burden associated with H7N9 infections.
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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.