ArticlePloS one2014
Major and minor group rhinoviruses elicit differential signaling and cytokine responses as a function of receptor-mediated signal transduction.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Rhinovirus Infects B and CD4 T Lymphocytes in Hypertrophic Tonsils in Children.Journal of medical virology · 2026Article
- Antiviral Activity of Rhamnolipids Nano-Micelles Against Rhinoviruses-In Silico Docking, Molecular Dynamic Analysis and In-Vitro Studies.Current issues in molecular biology · 2025Article
- Human rhinovirus 16 induces an ICAM-1-PKR-ATF2 axis to modulate macrophage functions.Journal of virology · 2024Article
- Host-directed therapy with 2-deoxy-D-glucose inhibits human rhinoviruses, endemic coronaviruses, and SARS-CoV-2.Journal of virus eradication · 2022Article
- Human rhinovirus serotypes induces different immune responses.Virology journal · 2021Article
- Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice.Mucosal immunology · 2021Article
- Kakkonto Inhibits Cytokine Production Induced by Rhinovirus Infection in Primary Cultures of Human Nasal Epithelial Cells.Frontiers in pharmacology · 2021Article
- Rhinovirus C Infection Induces Type 2 Innate Lymphoid Cell Expansion and Eosinophilic Airway Inflammation.Frontiers in immunology · 2021Article
- An investigation of rhinovirus infection on cellular uptake of poly (glycerol-adipate) nanoparticles.International journal of pharmaceutics · 2020Article
- Airway Epithelial Cells Generate Pro-inflammatory Tenascin-C and Small Extracellular Vesicles in Response to TLR3 Stimuli and Rhinovirus Infection.Frontiers in immunology · 2019Article
- Gene expression patterns induced at different stages of rhinovirus infection in human alveolar epithelial cells.PloS one · 2017Article
- Mechanism of human rhinovirus infections.Molecular and cellular pediatrics · 2016Review
- Interferon response of the cystic fibrosis bronchial epithelium to major and minor group rhinovirus infection.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2016Article
- Rhinoviruses and Their Receptors: Implications for Allergic Disease.Current allergy and asthma reports · 2016Review
- Article
- Clinical, virological and epidemiological characteristics of rhinovirus infections in early childhood: A comparison between non-hospitalised and hospitalised children.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2015Article
- NEMix: single-cell nested effects models for probabilistic pathway stimulation.PLoS computational biology · 2015Article
- Variation in the nuclear effects of infection by different human rhinovirus serotypes.Frontiers in microbiology · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Major- and minor-group human rhinoviruses (HRV) enter their host by binding to the cell surface molecules ICAM-1 and LDL-R, respectively, which are present on both macrophages and epithelial cells. Although epithelial cells are the primary site of productive HRV infection, previous studies have implicated macrophages in establishing the cytokine dysregulation that occurs during rhinovirus-induced asthma exacerbations. Analysis of the transcriptome of primary human macrophages exposed to major- and minor-group HRV demonstrated differential gene expression. Alterations in gene expression were traced to differential mitochondrial activity and signaling pathway activation between two rhinovirus serotypes, HRV16 (major-group) and HRV1A (minor-group), upon initial HRV binding. Variances in phosphorylation of kinases (p38, JNK, ERK5) and transcription factors (ATF-2, CREB, CEBP-alpha) were observed between the major- and minor-group HRV treatments. Differential activation of signaling pathways led to changes in the production of the asthma-relevant cytokines CCL20, CCL2, and IL-10. This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages, suggesting that receptor use is a mechanism for establishing the inflammatory microenvironment in the human airway upon exposure to rhinovirus.
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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.