Introduction: Poor lung health in children born prematurely is associated with severe viral infection during early life. An altered response of the airway epithelium, which acts as the frontline defence against foreign pathogens, may underpin severe infection. This study aimed to determine if nasal epithelial cells from preterm infants display a defective viral response compared to term infants.

Methods: Primary epithelial cultures were established and infected with human rhinovirus 1b (hRV1b) and respiratory syncytial virus (RSV). Barrier integrity was measured via transepithelial electrical resistance (TEER) and fluorescent permeability assays. Collected supernatant and RNA was analysed via ELISA and qPCR, for characterisation of caspase genes, viral load, viral receptors, and inflammatory mediators.

Results: Successful differentiation occurred in 90% of term samples (final n=9, 2.75±0.55 years) but only 52% of preterm samples (final n=12, 1.38±0.09 years). Preterm ALI cultures were more permeable at baseline (4.3cm/sec vs 9.9cm/sec, p<0.05), however TEER did not differ between cohorts (p>0.05). Interestingly, baseline cytokine concentrations were elevated in preterm cultures (IL-8: 5908pg/mL vs 4242pg/mL, p<0.05; CCL5: 37.04pg/mL vs 32.00pg/mL, p<0.01). Following infection, no difference was detected in cell lysis, apoptosis, viral receptor expression, inflammation, viral replication, permeability or TEER between term and preterm samples under tested conditions.

Conclusion: Preliminary data suggests certain viral-specific responses do not differ between term and preterm epithelial cells. However, underlying differences in inflammation and permeability may alter infection outcomes in those born preterm.