ArticleThe Journal of general virology2014
Highly pathogenic avian influenza A H5N1 and pandemic H1N1 virus infections have different phenotypes in Toll-like receptor 3 knockout mice.
Article in The Journal of general virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Suppression of the Toll-like receptors 3 mediated pro-inflammatory gene expressions by progenitor cell differentiation and proliferation factor in chicken DF-1 cells.Journal of animal science and technology · 2022Article
- Toll-like receptor 3 (TLR3) regulation mechanisms and roles in antiviral innate immune responses.Journal of Zhejiang University. Science. B · 2021Review
- Neutrophils in respiratory viral infections.Mucosal immunology · 2021Review
- Avian Toll-like receptor 3 isoforms and evaluation of Toll-like receptor 3-mediated immune responses using knockout quail fibroblast cells.Poultry science · 2020Article
- Review
- How the Respiratory Epithelium Senses and Reacts to Influenza Virus.American journal of respiratory cell and molecular biology · 2019Review
- The dual role of innate immunity during influenza.Biomedical journal · 2019Review
- The role of respiratory epithelium in host defence against influenza virus infection.Biomedical journal · 2018Review
- Innate Immunity Induces the Accumulation of Lung Mast Cells During Influenza Infection.Frontiers in immunology · 2018Article
- Advancements in Host-Based Interventions for Influenza Treatment.Frontiers in immunology · 2018Review
- HCFC2 is needed for IRF1- and IRF2-dependentThe Journal of experimental medicine · 2017Article
- A Role for Neutrophils in Viral Respiratory Disease.Frontiers in immunology · 2017Review
- CLEC5A-Mediated Enhancement of the Inflammatory Response in Myeloid Cells Contributes to Influenza Virus Pathogenicity In Vivo.Journal of virology · 2017Article
- --LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation.The Journal of experimental medicine · 2016Article
- Novel strategies for targeting innate immune responses to influenza.Mucosal immunology · 2016Article
- Human mesenchymal stromal cells reduce influenza A H5N1-associated acute lung injury in vitro and in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A20 Deficiency in Lung Epithelial Cells Protects against Influenza A Virus Infection.PLoS pathogens · 2016Article
- Host genes and influenza pathogenesis in humans: an emerging paradigm.Current opinion in virology · 2015Review
- Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus.Virology · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Toll-like receptors (TLRs) play an important role in innate immunity to virus infections. We investigated the role of TLR3 in the pathogenesis of H5N1 and pandemic H1N1 (pH1N1) influenza virus infections in mice. Wild-type mice and those defective in TLR3 were infected with influenza A/HK/486/97 (H5N1) or A/HK/415742/09 (pH1N1) virus. For comparison, mice defective in the gene for myeloid differential factor 88 (MyD88) were also infected with the viruses, because MyD88 signals through a TLR pathway different from TLR3. Survival and body weight loss were monitored for 14 days, and lung pathology, the lung immune-cell profile, viral load and cytokine responses were studied. H5N1-infected TLR3(-/-) mice had better survival than H5N1-infected WT mice, evident by significantly faster regain of body weight, lower viral titre in the lung and fewer pathological changes in the lung. However, this improved survival was not seen upon pH1N1 infection of TLR3(-/-) mice. In contrast, MyD88(-/-) mice had an increased viral titre and decreased leukocyte infiltration in the lungs after infection with H5N1 virus and poorer survival after pH1N1 infection. In conclusion, TLR3 worsens the pathogenesis of H5N1 infection but not of pH1N1 infection, highlighting the differences in the pathogenesis of these two viruses and the different roles of TLR3 in their 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 OpenQuestion graph.