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Updated: Mar 3, 2026

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Rhinovirus C targets ciliated airway epithelial cells
Theodor F Griggs1,2,3, Yury A Bochkov4, Sarmila Basnet4
1Department of Pediatrics, School of Medicine and Public Health, CSC K4/945, 600 Highland Ave, Madison, 53792, WI, USA. tgriggs@wisc.edu.
Rhinovirus C (RV-C) primarily infects and replicates in ciliated airway epithelial cells (AECs), leading to cell shedding. Cadherin related family member 3 (CDHR3) expression on ciliated AECs is key for RV-C binding and replication.
Area of Science:
- Virology
- Cell Biology
- Respiratory Medicine
Background:
- Rhinovirus C (RV-C) causes significant illness in children and asthmatics.
- The specific airway cells targeted by RV-C have remained unidentified.
- Hypotheses proposed ciliated airway epithelial cells (AECs) as the primary target, mediated by cadherin related family member 3 (CDHR3).
Purpose of the Study:
- To determine the primary host cell type for RV-C infection in the airways.
- To investigate the role of CDHR3 in RV-C cell entry and tropism.
Main Methods:
- Infection of differentiated human bronchial epithelial cell (HBEC) cultures with RV-C15.
- Assessment using immunofluorescent and time-lapse epifluorescent imaging.
- Immunohistochemistry to evaluate cell morphology and marker expression.
Main Results:
- RV-C15 infection was observed in ciliated AECs, not goblet cells.
- Infected cells showed increased staining for ciliated cell markers and were shed from the epithelium.
- CDHR3 expression was significantly higher on ciliated AECs and correlated with RV-C binding and replication.
Conclusions:
- RV-C replicates exclusively in ciliated AECs in vitro, resulting in cell shedding.
- CDHR3 expression on ciliated AECs is crucial for RV-C tropism and replication.
- Factors influencing AEC differentiation and CDHR3 production may dictate RV-C disease severity.
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