ArticleCell death & disease2023
Influenza viral matrix 1 protein aggravates viral pathogenicity by inducing TLR4-mediated reactive oxygen species production and apoptotic cell death.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Roles of progestogens in influenza A virus-induced inflammatory responses.Science China. Life sciences · 2026Article
- Redox-Dependent Activation of Matrix Metalloproteinases Regulates Influenza A Virus Replication in Neuronal Cells.International journal of microbiology · 2026Article
- Pre-activation timing determines influenza severity and viral pathogenicity via STING Inhibition.Scientific reports · 2025Article
- Exposure to bacterial lipopolysaccharide aggravates H1N1-mediated lung immunopathology via neutrophil extracellular trap formation.Scientific reports · 2025Article
- A novel C-3-substituted oleanolic acid benzyl amide derivative exhibits therapeutic potential against influenza A by targeting PA-PB1 interactions and modulating host macrophage inflammation.Acta pharmaceutica Sinica. B · 2025Article
- A5-A dual-target antiviral compound that rewrites the rules of influenza therapy.Acta pharmaceutica Sinica. B · 2025Article
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Article
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Oxidative Stress Induced by Antivirals: Implications for Adverse Outcomes During Pregnancy and in Newborns.Antioxidants (Basel, Switzerland) · 2024Review
- Age-related STING suppression in macrophages contributes to increased viral load during influenza a virus infection.Immunity & ageing : I & A · 2024Article
- H9N2 Avian Influenza Virus Downregulates FcRY Expression in Chicken Macrophage Cell Line HD11 by Activating the JNK MAPK Pathway.International journal of molecular sciences · 2024Article
- Mitochondrial Reactive Oxygen Species in TRIF-Dependent Toll-like Receptor 3 Signaling in Bronchial Epithelial Cells against Viral Infection.International journal of molecular sciences · 2023Article
- Generation of "OP7 chimera" defective interfering influenza A particle preparations free of infectious virus that show antiviral efficacy in mice.Scientific reports · 2023Article
- Serum Bilirubin Levels and Risk of Venous Thromboembolism among Influenza Patients: A Cohort Study.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Influenza virus is one of the most challenging viruses threating human health. Since infection with influenza virus triggers inflammatory responses and induces cell death, the molecular and cellular mechanisms by which the virus-infected cells undergo apoptotic and necrotic cell death have been widely studied. However, most of the studies have focused on the molecular events occurring in the cytosol and there is limited information on the physiological correlation between virus-induced cell death and the viral pathogenesis in vivo. In this study, we demonstrate that the influenza virus matrix 1 (M1) protein is released from virus-infected cells and triggers apoptotic cell death of lung epithelial and pulmonary immune cells, through the activation of Toll-like receptor 4 (TLR4) signaling. Treatment with M1 protein led to robust cellular inflammatory responses, such as the production of proinflammatory cytokines and cellular reactive oxygen species (ROS), and induction of cell death. When M1 protein was administered in vivo, it induced the activation of inflammatory responses and cell death in the lungs. Furthermore, the administration of M1 aggravated lung pathology and mortality of the virus-infected mice in a TLR4-dependent manner. These results demonstrate that M1 is an important pathogenic factor contributing to influenza virus pathogenicity by enhancing cell death in the lungs, thereby expanding our understanding of the molecular mechanism of influenza virus-induced cell death through the interaction with an innate immune receptor.
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