ArticleScientific reports2017
The H7N9 influenza A virus infection results in lethal inflammation in the mammalian host via the NLRP3-caspase-1 inflammasome.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 51 citations in OpenAlex.
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- H6N6 Avian Influenza Virus Infection Induced Pyroptosis of M1 Macrophages by Activating Caspase-1.Viruses · 2025Article
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- An interferon-stimulated long non-coding RNA USP30-AS1 as an immune modulator in influenza A virus infection.PLoS pathogens · 2025Article
- CD147 mediates the adsorption of influenza A virus on the cell surface through direct interaction with HA.Frontiers in cellular and infection microbiology · 2025Article
- 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
- Need for standardization of Influenza A virus-induced cell death in vivo to improve consistency of inter-laboratory research findings.Cell death discovery · 2024Review
- Article
- Review
- ZBP1/DAI-Dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Race between virus and inflammasomes: inhibition or escape, intervention and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.Viruses · 2022Review
- Comparing the Cytokine Storms of COVID-19 and Pandemic Influenza.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Article
- Review
- Uterus globulin associated protein 1 (UGRP1) binds podoplanin (PDPN) to promote a novel inflammation pathway during Streptococcus pneumoniae infection.Clinical and translational medicine · 2022Article
- Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death.Frontiers in immunology · 2022Article
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The avian origin influenza A virus (IAV) H7N9 has caused a considerable number of human infections associated with high rates of death since its emergence in 2013. As a vital component of the host innate immune system, the nucleotide-binding domain leucine-rich repeat containing receptor, pyrin domain containing 3 (NLRP3) inflammasome plays a critical role against H1N1 viral infection. However, the function of NLRP3 inflammasome in host immunological responses to the lethal H7N9 virus is still obscure. Here, we demonstrated that mice deficient for NLRP3 inflammasome components, including NLRP3, caspase-1, and Apoptosis-associated speck-like protein containing a CARD (ASC), were less susceptible to H7N9 viral challenge than wild type (WT) controls. Inflammasome deficiency in these animals led to significantly milder mortality and less pulmonary inflammation compared with WT mice. Furthermore, IL-1 receptor deficient mice also exhibited a higher survival rate than WT controls. Thus, our study reveals that the NLRP3 inflammasome is deleterious for the host during H7N9 infection in mice, which is due to an overwhelming inflammatory response via caspase-1 activation and associated IL-1 signal. Therefore, fine-tuning the activity of NLRP3 inflammasome or IL-1 signaling may be beneficial for the host to control H7N9 associated lethal pathogenesis.
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