ArticlePLoS pathogens2022
Rhinovirus C replication is associated with the endoplasmic reticulum and triggers cytopathic effects in an in vitro model of human airway epithelium.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- A robust cell-based infection model for Rhinovirus C research and antiviral drug discovery.Npj viruses · 2026Article
- Single-cell disentangled representations for perturbation modeling and treatment effect estimation.bioRxiv : the preprint server for biology · 2026Article
- Article
- Broad-spectrum host-targeting antivirals for rhinovirus infections: mechanisms and future perspectives.Frontiers in immunology · 2026Review
- Anti-SARS-CoV-2 Small Molecule Targeting of Oxysterol-Binding Protein (OSBP) Activates Cellular Antiviral Innate Immunity.ACS infectious diseases · 2025Article
- Review
- Investigation of Differentiated Nasal Epithelial Responses to Infection with Clinical Isolates of Rhinovirus A and C.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Protective effect of interferon type I on barrier function of human airway epithelium during rhinovirus infections in vitro.Scientific reports · 2024Article
- Human Stimulator of Interferon Genes Promotes Rhinovirus C Replication in Mouse Cells In Vitro and In Vivo.Viruses · 2024Article
- A Rapid-Patterning 3D Vessel-on-Chip for Imaging and Quantitatively Analyzing Cell-Cell Junction Phenotypes.Bioengineering (Basel, Switzerland) · 2023Article
- Remember the Airway Smooth Muscle! How Rhinovirus Impairs Bronchodilator Responses.American journal of respiratory cell and molecular biology · 2023Article
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- YAP inhibits HCMV replication by impairing STING-mediated nuclear transport of the viral genome.PLoS pathogens · 2022Article
- MUC5B mobilizes and MUC5AC spatially aligns mucociliary transport on human airway epithelium.Science advances · 2022Article
- Immunofluorescence-Mediated Detection of Respiratory Virus Infections in Human Airway Epithelial Cultures.Current protocols · 2022Article
- Rhinoviruses usurp STING for replication.Nature microbiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The clinical impact of rhinovirus C (RV-C) is well-documented; yet, the viral life cycle remains poorly defined. Thus, we characterized RV-C15 replication at the single-cell level and its impact on the human airway epithelium (HAE) using a physiologically-relevant in vitro model. RV-C15 replication was restricted to ciliated cells where viral RNA levels peaked at 12 hours post-infection (hpi), correlating with elevated titers in the apical compartment at 24hpi. Notably, infection was associated with a loss of polarized expression of the RV-C receptor, cadherin-related family member 3. Visualization of double-stranded RNA (dsRNA) during RV-C15 replication revealed two distinct replication complex arrangements within the cell, likely corresponding to different time points in infection. To further define RV-C15 replication sites, we analyzed the expression and colocalization of giantin, phosphatidylinositol-4-phosphate, and calnexin with dsRNA. Despite observing Golgi fragmentation by immunofluorescence during RV-C15 infection as previously reported for other RVs, a high ratio of calnexin-dsRNA colocalization implicated the endoplasmic reticulum as the primary site for RV-C15 replication in HAE. RV-C15 infection was also associated with elevated stimulator of interferon genes (STING) expression and the induction of incomplete autophagy, a mechanism used by other RVs to facilitate non-lytic release of progeny virions. Notably, genetic depletion of STING in HAE attenuated RV-C15 and -A16 (but not -B14) replication, corroborating a previously proposed proviral role for STING in some RV infections. Finally, RV-C15 infection resulted in a temporary loss in epithelial barrier integrity and the translocation of tight junction proteins while a reduction in mucociliary clearance indicated cytopathic effects on epithelial function. Together, our findings identify both shared and unique features of RV-C replication compared to related rhinoviruses and define the impact of RV-C on both epithelial cell organization and tissue functionality-aspects of infection that may contribute to pathogenesis in vivo.
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