ArticleJournal of virology2012
Cholesterol-rich microdomains as docking platforms for respiratory syncytial virus in normal human bronchial epithelial cells.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- 3D Single-Virus Tracking: Advances in Methodology and Labeling Strategies Towards Probing the Virus-Epithelium Interaction.Viruses · 2026Review
- STAT1 signaling controls cholesterol metabolism in epithelial cells and RSV-induced syncytia formation.Npj viruses · 2026Article
- Review
- Cholesterol-rich lipid rafts mediate endocytosis as a common pathway for respiratory syncytial virus entry into different host cells.Microbiology spectrum · 2025Article
- Internalization-related host factors of common respiratory viruses.Frontiers in immunology · 2025Review
- Respiratory syncytial virus fuses with plasma membrane to infect primary cultures of bronchial epithelial cells.Frontiers in microbiology · 2025Article
- How a paramyxovirus fusion/entry complex adapts to escape a neutralizing antibody.Nature communications · 2024Article
- Cholesterol-rich lysosomes induced by respiratory syncytial virus promote viral replication by blocking autophagy flux.Nature communications · 2024Article
- Identification and Analysis of Biomarkers Associated with Lipophagy and Therapeutic Agents for COVID-19.Viruses · 2024Article
- Detailed analysis of low temperature inactivation of respiratory syncytial virus.Scientific reports · 2024Article
- Hypoxia inducible factors inhibit respiratory syncytial virus infection by modulation of nucleolin expression.iScience · 2024Article
- Exploring the secrets of virus entry: the first respiratory syncytial virus carrying beta lactamase.Frontiers in microbiology · 2024Article
- Actin cytoskeleton remodeling disrupts physical barriers to infection and presents entry receptors to respiratory syncytial virus.The Journal of general virology · 2023Article
- Cholesterol-Lowering Drugs as Potential Antivirals: A Repurposing Approach against Flavivirus Infections.Viruses · 2023Article
- The RSV F p27 peptide: current knowledge, important questions.Frontiers in microbiology · 2023Review
- Multiple Respiratory Syncytial Virus (RSV) Strains Infecting HEp-2 and A549 Cells Reveal Cell Line-Dependent Differences in Resistance to RSV Infection.Journal of virology · 2022Article
- Antibody responses of healthy adults to the p27 peptide of respiratory syncytial virus fusion protein.Vaccine · 2022Article
- Statin-mediated disruption of Rho GTPase prenylation and activity inhibits respiratory syncytial virus infection.Communications biology · 2021Article
- Roles of Cholesterol in Early and Late Steps of the Nipah Virus Membrane Fusion Cascade.Journal of virology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
Abstract
Respiratory syncytial virus (RSV) is one of the major causes of respiratory infections in children, and it is the main pathogen causing bronchiolitis in infants. The binding and entry mechanism by which RSV infects respiratory epithelial cells has not yet been determined. In this study, the earliest stages of RSV infection in normal human bronchial epithelial cells were probed by tracking virions with fluorescent lipophilic dyes in their membranes. Virions colocalized with cholesterol-containing plasma membrane microdomains, identified by their ability to bind cholera toxin subunit B. Consistent with an important role for cholesterol in RSV infection, cholesterol depletion profoundly inhibited RSV infection, while cholesterol repletion reversed this inhibition. Merger of the outer leaflets of the viral envelope and the cell membrane appeared to be triggered at these sites. Using small-molecule inhibitors, RSV infection was found to be sensitive to Pak1 inhibition, suggesting the requirement of a subsequent step of cytoskeletal reorganization that could involve plasma membrane rearrangements or endocytosis. It appears that RSV entry depends on its ability to dock to cholesterol-rich microdomains (lipid rafts) in the plasma membrane where hemifusion events begin, assisted by a Pak1-dependent process.
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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.