Relative Respiratory Syncytial Virus Cytopathogenesis in Upper and Lower Respiratory Tract Epithelium

Hong Guo-Parke, Paul Canning, Isobel Douglas, Rémi Villenave, Liam G. Heaney, Peter V. Coyle, Jeremy D. Lyons, Michael D. Shields, Ultan F. Power
  • American Review of Respiratory Disease, October 2013, American Thoracic Society
  • DOI: 10.1164/rccm.201304-0750oc

What is it about?

Respiratory syncytial virus (RSV) is the main cause of severe lung disease, such as bronchiolitis, in young infants. It primarily infects and replicates in the airway epithelium. It is a descending infection that starts in the upper respiratory tract and progresses to the lower respiratory tract. RSV infection of well-differentiated paediatric primary bronchial epithelial cells (WD-PBECs) reproduces many of the hallmarks of RSV pathogenesis in infants. However, there is very little literature on RSV cytopathogenesis in the upper airways and none directly comparing this cytopathogenesis in upper and lower respiratory tract airway epithelium from the same individuals. We describe a novel model of RSV cytopathogenesis based on morphologically and physiologically authentic well-differentiated pediatric primary nasal epithelial cells (WD-PNECs) derived from nasal brushes. We demonstrate that this RSV/WD-PNEC model replicates many of the hallmarks of RSV cytopathogenesis evident in WD-PBECs derived from the same individuals, and RSV pathogenesis in infants. As such, WD-PNECs may provide appropriate surrogates for WD-PBECs with which to study RSV-human airway epithelium interactions.

Why is it important?

Our new model, coupled with the relative ease of access to infant nasal epithelial cells, opens the potential to study RSV pathogenesis in airway epithelium derived from different infant cohorts and also the therapeutic potential of novel pharmaceuticals against RSV in a physiologically authentic culture system.

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The following have contributed to this page: Prof. Ultan F Power