Abstract
Chronic lung disease remains the primary cause of mortality in cystic fibrosis (CF). Growing evidence suggests respiratory viral infections are often more severe in CF compared to healthy peers and contributes to pulmonary exacerbations (PEx) and deterioration of lung function. Rhinovirus is the most prevalent respiratory virus detected, particularly during exacerbations in children with CF <5 years old. However, even though rhinoviral infections are likely to be one of the factors initiating the onset of CF lung disease, there is no effective targeted treatment. A better understanding of the innate immune responses by CF airway epithelial cells, the primary site of infection for viruses, is needed to identify why viral infections are more severe in CF. The aim of this review is to present the clinical impact of virus infection in both young children and adults with CF, focusing on rhinovirus infection. Previous in vitro and in vivo investigations looking at the mechanisms behind virus infection will also be summarized. The review will finish on the potential of transcriptomics to elucidate the host-pathogen responses by CF airway cells to viral infection and identify novel therapeutic targets.
Highlights
Elucidating the Interaction of cystic fibrosis (CF) Airway Epithelial Cells and Rhinovirus: Using the Host-Pathogen Relationship to Identify Future Therapeutic Strategies
The aim of this review is to present the clinical impact of virus infection in both young children and adults with CF, focusing on rhinovirus infection
RV infection remains a significant cause of pulmonary exacerbation in CF
Summary
Elucidating the Interaction of CF Airway Epithelial Cells and Rhinovirus: Using the Host-Pathogen Relationship to Identify Future Therapeutic Strategies. Chronic lung disease remains the primary cause of mortality in cystic fibrosis (CF). The review will finish on the potential of transcriptomics to elucidate the host-pathogen responses by CF airway cells to viral infection and identify novel therapeutic targets. The defective function of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene initiates a lifelong cycle of neutrophilic inflammation, progressive bronchiectasis, mucus obstruction and recurrent microbial infection of the CF airway. These processes typically begin in the first years of life and lead to eventual lung failure during early adulthood. The CF airway environment is vulnerable to colonization by particular bacterial
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