ArticleJournal of virology2013
The respiratory syncytial virus fusion protein and neutrophils mediate the airway mucin response to pathogenic respiratory syncytial virus infection.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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.
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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
71 citing papers in PubMed, 105 citations in OpenAlex.
- Potential effects of genetic variations in fusion protein on the virulence of human respiratory syncytial virus.Frontiers in immunology · 2026Article
- βNature communications · 2025Article
- B-Raf kinase blockade protects airway epithelial cells against respiratory syncytial virus infection and modulates interferon responses.ERJ open research · 2025Article
- Guideline for the diagnosis, treatment, and prevention of respiratory syncytial virus infection in children in China.Pediatric investigation · 2025Article
- Clinical characteristics of single human rhinovirus infection and co-infection in the respiratory tract of children.Translational pediatrics · 2025Article
- Short-Chain Fatty Acids: Promising Therapeutic Targets for Respiratory Syncytial Virus Infection.Clinical reviews in allergy & immunology · 2025Review
- Lethal model for respiratory syncytial virus infection using C57BL/6 mice.Journal of virology · 2024Article
- Distinct roles for type I and type III interferons in virulent human metapneumovirus pathogenesis.PLoS pathogens · 2024Article
- Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity.Cells · 2023Review
- Article
- Impact of genetic polymorphisms related to innate immune response on respiratory syncytial virus infection in children.Virus genes · 2022Review
- Influence of SARS-CoV-2 on airway mucus production: A review and proposed model.Veterinary pathology · 2022Review
- A prolonged innate systemic immune response in COVID-19.Scientific reports · 2022Article
- Neutrophil subsets and their differential roles in viral respiratory diseases.Journal of leukocyte biology · 2022Review
- Role of neutrophils in acute viral infection.Immunity, inflammation and disease · 2021Review
- Review
- Neutrophils in respiratory viral infections.Mucosal immunology · 2021Review
- Review
- Cytokine Storm and Mucus Hypersecretion in COVID-19: Review of Mechanisms.Journal of inflammation research · 2021Review
- Abnormal Airway Mucus Secretion Induced by Virus Infection.Frontiers in immunology · 2021Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Respiratory syncytial virus (RSV) is the leading cause of death due to a viral etiology in infants. RSV disease is characterized by epithelial desquamation, neutrophilic bronchiolitis and pneumonia, and obstructive pulmonary mucus. It has been shown that infection of BALB/cJ mice with RSV clinical isolate A2001/2-20 (2-20) results in a higher early viral load, greater airway necrosis, and higher levels of interleukin-13 (IL-13) and airway mucin expression than infection with RSV laboratory strain A2. We hypothesized that the fusion (F) protein of RSV 2-20 is a mucus-inducing viral factor. In vitro, the fusion activity of 2-20 F but not that of A2 F was enhanced by expression of RSV G. We generated a recombinant F-chimeric RSV by replacing the F gene of A2 with the F gene of 2-20, generating A2-2-20F. Similar to the results obtained with the parent 2-20 strain, infection of BALB/cJ mice with A2-2-20F resulted in a higher early viral load and higher levels of subsequent pulmonary mucin expression than infection with the A2 strain. A2-2-20F infection induced greater necrotic airway damage and neutrophil infiltration than A2 infection. We hypothesized that the neutrophil response to A2-2-20F infection is involved in mucin expression. Antibody-mediated depletion of neutrophils in RSV-infected mice resulted in lower tumor necrosis factor alpha levels, fewer IL-13-expressing CD4 T cells, and less airway mucin production in the lung. Our data are consistent with a model in which the F and attachment (G) glycoprotein functional interaction leads to enhanced fusion and F is a key factor in airway epithelium infection, pathogenesis, and subsequent airway mucin expression.
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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.