ArticleJournal of innate immunity2016
Alveolar Macrophages Can Control Respiratory Syncytial Virus Infection in the Absence of Type I Interferons.
Article in Journal of innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 66 citations in OpenAlex.
- Macrophages orchestrate antiviral defense and epithelial repair in a human iPSC-derived alveolar air-liquid interface.JCI insight · 2026Article
- Type I interferons induced upon respiratory viral infection impair lung metastatic initiation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Suppression of Nr1d1/Bnip3-dependent mitophagy by notch signaling aggravates inflammatory response in RSV-infected mice lungs.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The Complexity of Immunoglobulin A Immune Responses in Respiratory Syncytial Virus Infection.Viruses · 2026Review
- Review
- Enhanced Pathogenic Consequences Induced by a Seven-Amino-Acid Extension in the G Protein of the HRSV BA9 Genotype.International journal of molecular sciences · 2025Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Analysis of BeyfortusCurrent issues in molecular biology · 2024Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- Dampening of ISGylation of RIG-I by ADAP regulates type I interferon response of macrophages to RNA virus infection.PLoS pathogens · 2024Article
- Transcriptome profiling of macrophages persistently infected with human respiratory syncytial virus and effect of recombinantFrontiers in microbiology · 2024Article
- Respiratory viral infection and resolution of inflammation: Roles for specialized pro-resolving mediators.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Host Responses to Respiratory Syncytial Virus Infection.Viruses · 2023Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- TLR7 promotes chronic airway disease in RSV-infected mice.Frontiers in immunology · 2023Article
- Tissue-resident immunity in the lung: a first-line defense at the environmental interface.Seminars in immunopathology · 2022Review
- Review
- Early innate immune response triggered by the human respiratory syncytial virus and its regulation by ubiquitination/deubiquitination processes.Journal of biomedical science · 2022Review
- Can bacterial lysates be useful in prevention of viral respiratory infections in childhood? The results of experimental OM-85 studies.Frontiers in pediatrics · 2022Review
- Alveolar macrophages and airway hyperresponsiveness associated with respiratory syncytial virus infection.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract infections. Immunity to RSV is initiated upon detection of the virus by pattern recognition receptors, such as RIG-I-like receptors. RIG-I-like receptors signal via MAVS to induce the synthesis of proinflammatory mediators, including type I interferons (IFNs), which trigger and shape antiviral responses and protect cells from infection. Alveolar macrophages (AMs) are amongst the first cells to encounter invading viruses and the ones producing type I IFNs. However, it is unclear whether IFNs act to prevent AMs from serving as vehicles for viral replication. In this study, primary AMs from MAVS (Mavs-/-)- or type I IFN receptor (Ifnar1-/-)-deficient mice were exposed to RSV ex vivo. Wild-type (wt) AMs but not Mavs-/- and Ifnar1-/- AMs produced inflammatory mediators in response to RSV. Furthermore, Mavs-/- and Ifnar1-/- AMs accumulated more RSV proteins than wt AMs, but the infection was abortive. Thus, RIG-I-like receptor-MAVS and IFNAR signalling are important for the induction of proinflammatory mediators from AMs upon RSV infection, but this signalling is not central for controlling viral replication. The ability to restrict viral replication makes AMs ideal sensors of RSV infection and important initiators of immune responses in the lung.
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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.