ArticleThe Journal of infectious diseases2018
1918 H1N1 Influenza Virus Replicates and Induces Proinflammatory Cytokine Responses in Extrarespiratory Tissues of Ferrets.
Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- A Systematic Review of the Neuropathologic Findings of Post-Viral Olfactory Dysfunction: Implications and Novel Insight for the COVID-19 Pandemic.American journal of rhinology & allergy · 2021Pooled it
- Decoding the lung-brain axis in influenza: from pulmonary infection to central nervous system injury.Journal of neuroinflammation · 2026Review
- Influenza A virus infection impairs neuronal activity in human iPSC-derived NGN2 neural co-cultures.Acta neuropathologica communications · 2026Article
- Febrile temperature activates the innate immune response by promoting aberrant influenza A virus RNA synthesis.Science advances · 2026Article
- Body Size and Risk of Death During the 1918 Influenza Pandemic in Alaska.American journal of human biology : the official journal of the Human Biology Council · 2025Article
- A two-step mechanism for RIG-I activation by influenza virus mvRNAs.Science advances · 2025Article
- Febrile temperature activates the innate immune response by promoting aberrant influenza A virus RNA synthesis.bioRxiv : the preprint server for biology · 2025Article
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Quantification of influenza virus mini viral RNAs using Cas13.RNA (New York, N.Y.) · 2024Article
- Quantification of influenza virus mini viral RNA dynamics using Cas13.bioRxiv : the preprint server for biology · 2024Article
- Comparative Pathology of Animal Models for Influenza A Virus Infection.Pathogens (Basel, Switzerland) · 2023Review
- The neuropathogenesis of highly pathogenic avian influenza H5Nx viruses in mammalian species including humans.Trends in neurosciences · 2023Review
- The pro-inflammatory response to influenza A virus infection is fueled by endothelial cells.Life science alliance · 2023Article
- Evolution of highly pathogenic H5N1 influenza A virus in the central nervous system of ferrets.PLoS pathogens · 2023Article
- Article
- In vitro and in vivo differences in neurovirulence between D614G, Delta And Omicron BA.1 SARS-CoV-2 variants.Acta neuropathologica communications · 2022Article
- Pandemic 1918 Influenza Virus Does Not Cause Lethal Infection in Rhesus or Cynomolgus Macaques.Journal of virology · 2022Article
- Efficacy of Combination Therapy with the JAK Inhibitor Baricitinib in the Treatment of COVID-19.SN comprehensive clinical medicine · 2022Article
- The influenza virus RNA polymerase as an innate immune agonist and antagonist.Cellular and molecular life sciences : CMLS · 2021Review
- The Potential Role of Cytokine Storm Pathway in the Clinical Course of Viral Respiratory Pandemic.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
Background: The 1918 Spanish H1N1 influenza pandemic was the most severe recorded influenza pandemic with an estimated 20-50 million deaths worldwide. Even though it is known that influenza viruses can cause extrarespiratory tract complications-which are often severe or even fatal-the potential contribution of extrarespiratory tissues to the pathogenesis of 1918 H1N1 virus infection has not been studied comprehensively. Methods: Here, we performed a time-course study in ferrets inoculated intranasally with 1918 H1N1 influenza virus, with special emphasis on the involvement of extrarespiratory tissues. Respiratory and extrarespiratory tissues were collected after inoculation for virological, histological, and immunological analysis. Results: Infectious virus was detected at high titers in respiratory tissues and, at lower titers in most extrarespiratory tissues. Evidence for active virus replication, as indicated by the detection of nucleoprotein by immunohistochemistry, was observed in the respiratory tract, peripheral and central nervous system, and liver. Proinflammatory cytokines were up-regulated in respiratory tissues, olfactory bulb, spinal cord, liver, heart, and pancreas. Conclusions: 1918 H1N1 virus spread to and induced cytokine responses in tissues outside the respiratory tract, which likely contributed to the severity of infection. Moreover, our data support the suggested link between 1918 H1N1 infection and central nervous system disease.
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