ArticleJournal of virology2021
Influenza Virus Neuraminidase Engages CD83 and Promotes Pulmonary Injury.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The gut-lung axis and viral pneumonia: Unrevealing the gut microbiota.Pharmaceutical science advances · 2026Review
- Desialylated vs. Oxidized LDL: Sialidase Inhibitors as Promising Antiatherosclerotic Agents.Current atherosclerosis reports · 2026Review
- Dextrorotatory kynurenine suppresses acute rejection through inhibiting M1 macrophage-mediated inflammation.EMBO molecular medicine · 2026Article
- Chronic Diseases and Influenza Vaccines.Vaccines · 2025Review
- Immune Responses of Dendritic Cells to Zoonotic DNA and RNA Viruses.Veterinary sciences · 2025Review
- Epigenetic changes and serotype-specific responses of alveolar type II epithelial cells to Streptococcus pneumoniae in resolving influenza A virus infection.Cell communication and signaling : CCS · 2025Article
- Influenza Virus Genomic Mutations, Host Barrier and Cross-species Transmission.Current genomics · 2025Review
- [Inhibitory effect of 5-hydroxy-6,7-dimethoxyflavone on H1N1 influenza virus-induced ferroptosis and inflammation in A549 cells and its possible mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Pandemic influenza A (H1N1) virus causes abortive infection of primary human T cells.Emerging microbes & infections · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A viruses cause severe respiratory illnesses in humans and animals. Overreaction of the innate immune response to influenza virus infection results in hypercytokinemia, which is responsible for mortality and morbidity. However, the mechanism by which influenza induces hypercytokinemia is not fully understood. In this study, we established a mouse-adapted H9N2 virus, MA01, to evaluate the innate immune response to influenza in the lung. MA01 infection caused high levels of cytokine release, enhanced pulmonary injury in mice, and upregulated CD83 protein in dendritic cells and macrophages in the lung. Influenza virus neuraminidase (NA) unmasked CD83 protein and contributed to high cytokine levels. Furthermore, we provide evidence that CD83 is a sialylated glycoprotein. Neuraminidase treatment enhanced lipopolysaccharide (LPS)-stimulated NF-κB activation in RAW264.7 cells. Anti-CD83 treatment alleviated influenza virus-induced lung injury in mice. Our study indicates that influenza virus neuraminidase modulates CD83 status and contributes to the "cytokine storm," which may suggest a new approach to curb this immune injury.
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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.