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Peer-reviewedCC BYRespiratory Research

Rhinovirus C targets ciliated airway epithelial cells

  • T. F. Griggs
  • Y. A. Bochkov
  • S. Basnet
  • T. R. Pasic
  • R. A. Brockman-Schneider
  • A. C. Palmenberg
  • J. E. Gern
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Abstract

BACKGROUND: The Rhinovirus C (RV-C), first identified in 2006, produce high symptom burdens in children and asthmatics, however, their primary target host cell in the airways remains unknown. Our primary hypotheses were that RV-C target ciliated airway epithelial cells (AECs), and that cell specificity is determined by restricted and high expression of the only known RV-C cell-entry factor, cadherin related family member 3 (CDHR3). METHODS: RV-C15 (C15) infection in differentiated human bronchial epithelial cell (HBEC) cultures was assessed using immunofluorescent and time-lapse epifluorescent imaging. Morphology of C15-infected differentiated AECs was assessed by immunohistochemistry. RESULTS: C15 produced a scattered pattern of infection, and infected cells were shed from the epithelium. The percentage of cells infected with C15 varied from 1.4 to 14.7% depending on cell culture conditions. Infected cells had increased staining for markers of ciliated cells (acetylated-alpha-tubulin [aat], p < 0.001) but not markers of goblet cells (wheat germ agglutinin or Muc5AC, p = ns). CDHR3 expression was increased on ciliated epithelial cells, but not other epithelial cells (p < 0.01). C15 infection caused a 27.4% reduction of ciliated cells expressing CDHR3 (p < 0.01). During differentiation of AECs, CDHR3 expression progressively increased and correlated with both RV-C binding and replication. CONCLUSIONS: The RV-C only replicate in ciliated AECs in vitro, leading to infected cell shedding. CDHR3 expression positively correlates with RV-C binding and replication, and is largely confined to ciliated AECs. Our data imply that factors regulating differentiation and CDHR3 production may be important determinants of RV-C illness severity.

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Cite

BibTeXRIS
BibTeX
@article{griggs2026rhinovirus,
  title = {{Rhinovirus C targets ciliated airway epithelial cells}},
  author = {T. F. Griggs and Y. A. Bochkov and S. Basnet and T. R. Pasic and R. A. Brockman-Schneider and A. C. Palmenberg and J. E. Gern},
  journal = {Respiratory Research},
  year = {2026},
  month = oct,
  doi = {10.1186/s12931-017-0567-0},
  url = {https://hal.science/hal-05787874v1},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Rhinovirus C targets ciliated airway epithelial cells
AU  - T. F. Griggs
AU  - Y. A. Bochkov
AU  - S. Basnet
AU  - T. R. Pasic
AU  - R. A. Brockman-Schneider
AU  - A. C. Palmenberg
AU  - J. E. Gern
PY  - 2026
DA  - 2026/10/09
JO  - Respiratory Research
DO  - 10.1186/s12931-017-0567-0
UR  - https://hal.science/hal-05787874v1
AB  - BACKGROUND: The Rhinovirus C (RV-C), first identified in 2006, produce high symptom burdens in children and asthmatics, however, their primary target host cell in the airways remains unknown. Our primary hypotheses were that RV-C target ciliated airway epithelial cells (AECs), and that cell specificity is determined by restricted and high expression of the only known RV-C cell-entry factor, cadherin related family member 3 (CDHR3). METHODS: RV-C15 (C15) infection in differentiated human bronchial epithelial cell (HBEC) cultures was assessed using immunofluorescent and time-lapse epifluorescent imaging. Morphology of C15-infected differentiated AECs was assessed by immunohistochemistry. RESULTS: C15 produced a scattered pattern of infection, and infected cells were shed from the epithelium. The percentage of cells infected with C15 varied from 1.4 to 14.7% depending on cell culture conditions. Infected cells had increased staining for markers of ciliated cells (acetylated-alpha-tubulin [aat], p < 0.001) but not markers of goblet cells (wheat germ agglutinin or Muc5AC, p = ns). CDHR3 expression was increased on ciliated epithelial cells, but not other epithelial cells (p < 0.01). C15 infection caused a 27.4% reduction of ciliated cells expressing CDHR3 (p < 0.01). During differentiation of AECs, CDHR3 expression progressively increased and correlated with both RV-C binding and replication. CONCLUSIONS: The RV-C only replicate in ciliated AECs in vitro, leading to infected cell shedding. CDHR3 expression positively correlates with RV-C binding and replication, and is largely confined to ciliated AECs. Our data imply that factors regulating differentiation and CDHR3 production may be important determinants of RV-C illness severity.
SN  - 1465-9921
ER  -