ArticleJournal of virology2014
Delayed sequelae of neonatal respiratory syncytial virus infection are dependent on cells of the innate immune system.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 46 citations in OpenAlex.
- Catching our breath: development of interventions and therapies for respiratory syncytial virus.Microbiology and molecular biology reviews : MMBR · 2026Review
- Review
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Antibody-based protection against respiratory syncytial virus in mice and their offspring through vectored immunoprophylaxis.Gene therapy · 2025Article
- Lung-resident lymphocytes and their roles in respiratory infections and chronic respiratory diseases.Chinese medical journal pulmonary and critical care medicine · 2024Review
- The Neonatal Immune System and Respiratory Pathogens.Microorganisms · 2023Review
- Article
- Activation of cGAS-STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11bAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- IL-1β Promotes Expansion of IL-33American journal of respiratory cell and molecular biology · 2022Article
- Enhanced IL-2 in early life limits the development of TFH and protective antiviral immunity.The Journal of experimental medicine · 2021Article
- Depletion of TAX1BP1 Amplifies Innate Immune Responses during Respiratory Syncytial Virus Infection.Journal of virology · 2021Article
- TNF-mediated alveolar macrophage necroptosis drives disease pathogenesis during respiratory syncytial virus infection.The European respiratory journal · 2021Article
- Genetic influences on viral-induced cytokine responses in the lung.Mucosal immunology · 2021Review
- Article
- Innate Immune Components that Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections.Viruses · 2020Review
- Alveolar Macrophages Are Key Players in the Modulation of the Respiratory Antiviral Immunity Induced by Orally AdministeredFrontiers in immunology · 2020Article
- Respiratory Syncytial Virus Fusion Protein-encoding DNA Vaccine Is Less Effective in Conferring Protection against Inflammatory Disease than a Virus-like Particle Platform.Immune network · 2019Article
- Respiratory Syncytial Virus Infects Primary Neonatal and Adult Natural Killer Cells and Affects Their Antiviral Effector Function.The Journal of infectious diseases · 2019Article
- The switch between acute and persistent paramyxovirus infection caused by single amino acid substitutions in the RNA polymerase P subunit.PLoS pathogens · 2019Article
- Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Infection with respiratory syncytial virus (RSV) in neonatal mice leads to exacerbated disease if mice are reinfected with the same virus as adults. Both T cells and the host major histocompatibility complex genotype contribute to this phenomenon, but the part played by innate immunity has not been defined. Since macrophages and natural killer (NK) cells play key roles in regulating inflammation during RSV infection of adult mice, we studied the role of these cells in exacerbated inflammation following neonatal RSV sensitization/adult reinfection. Compared to mice undergoing primary infection as adults, neonatally sensitized mice showed enhanced airway fluid levels of interleukin-6 (IL-6), alpha interferon (IFN-α), CXCL1 (keratinocyte chemoattractant/KC), and tumor necrosis factor alpha (TNF-α) at 12 to 24 h after reinfection and IL-4, IL-5, IFN-γ, and CCL11 (eotaxin) at day 4 after reinfection. Weight loss during reinfection was accompanied by an initial influx of NK cells and granulocytes into the airways and lungs, followed by T cells. NK cell depletion during reinfection attenuated weight loss but did not alter T cell responses. Depletion of alveolar macrophages with inhaled clodronate liposomes reduced both NK and T cell numbers and attenuated weight loss. These findings indicate a hitherto unappreciated role for the innate immune response in governing the pathogenic recall responses to RSV infection.
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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.