ArticlePLoS pathogens2018
CDHR3 extracellular domains EC1-3 mediate rhinovirus C interaction with cells and as recombinant derivatives, are inhibitory to virus infection.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 26 citations in OpenAlex.
- Pediatric and adult primary human airway epithelia exhibit similar rhinovirus C replication, innate responses, and expression of protein receptor.Microbiology spectrum · 2026Article
- Optimized Propagation and Purification Protocols for Large-Scale Production of Rhinovirus C.Viruses · 2026Article
- Broad-spectrum host-targeting antivirals for rhinovirus infections: mechanisms and future perspectives.Frontiers in immunology · 2026Review
- Rhinovirus, an Age-Old Problem Yet to be Solved: A Comprehensive Review Discussing Modern Therapeutics.Health science reports · 2025Article
- Human Stimulator of Interferon Genes Promotes Rhinovirus C Replication in Mouse Cells In Vitro and In Vivo.Viruses · 2024Article
- Interactive effects betweenMicrobiology spectrum · 2023Article
- ACE2 and COVID-19 Susceptibility and Severity.Aging and disease · 2022Article
- Rhinovirus C replication is associated with the endoplasmic reticulum and triggers cytopathic effects in an in vitro model of human airway epithelium.PLoS pathogens · 2022Article
- The role of CDHR3 in susceptibility to otitis media.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Exploring the potential of foodborne transmission of respiratory viruses.Food microbiology · 2021Review
- Enhanced Neutralizing Antibody Responses to Rhinovirus C and Age-Dependent Patterns of Infection.American journal of respiratory and critical care medicine · 2021Article
- Article
- Rhinovirus C Infection Induces Type 2 Innate Lymphoid Cell Expansion and Eosinophilic Airway Inflammation.Frontiers in immunology · 2021Article
- Viral Induced Effects on a Vulnerable Epithelium; Lessons Learned From Paediatric Asthma and Eosinophilic Oesophagitis.Frontiers in immunology · 2021Review
- ELISA-Based Assay for Studying Major and Minor Group Rhinovirus-Receptor Interactions.Vaccines · 2020Article
- Cryo-EM structure of rhinovirus C15a bound to its cadherin-related protein 3 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Exacerbation-Prone Asthma.The journal of allergy and clinical immunology. In practice · 2020Article
- Rhinovirus and Innate Immune Function of Airway Epithelium.Frontiers in cellular and infection microbiology · 2020Review
- Rhinoviruses and Their Receptors.Chest · 2019Review
- Evolutionary and Structural Overview of Human Picornavirus Capsid Antibody Evasion.Frontiers in cellular and infection microbiology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Viruses in the rhinovirus C species (RV-C) are more likely to cause severe wheezing illnesses and asthma exacerbations in children than related isolates of the RV-A or RV-B. The RV-C capsid is structurally distinct from other rhinoviruses and does not bind ICAM-1 or LDL receptors. The RV-C receptor is instead, human cadherin-related family member 3 (CDHR3), a protein unique to the airway epithelium. A single nucleotide polymorphism (rs6967330, encoding C529Y) in CDHR3 regulates the display density of CDHR3 on cell surfaces and is among the strongest known genetic correlates for childhood virus-induced asthma susceptibility. CDHR3 immunoprecipitations from transfected or transduced cell lysates were used to characterize the RV-C interaction requirements. The C529 and Y529 variations in extracellular repeat domain 5 (EC5), bound equivalently to virus. Glycosylase treatment followed by mass spectrometry mapped 3 extracellular N-linked modification sites, and further detected surface-dependent, α2-6 sialyation unique to the Y529 format. None of these modifications were required for RV-C recognition, but removal or even dilution of structurally stabilizing calcium ions from the EC junctions irreversibly abrogated virus binding. CDHR3 deletions expressed in HeLa cells or as bacterial recombinant proteins, mapped the amino-terminal EC1 unit as the required virus contact. Derivatives containing the EC1 domain, could not only recapitulate virus:receptor interactions in vitro, but also directly inhibit RV-C infection of susceptible cells for several virus genotypes (C02, C15, C41, and C45). We propose that all RV-C use the same EC1 landing pad, interacting with putative EC3-mediated multimerization formats of CDHR3.
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