There is a growing body of evidence suggesting that respiratory pathogens can alter the ion transport and hence electrical properties of the respiratory epithelium. Severe respiratory syncytial virus (RSV) infection disturbs the fluid balance in the lower airways, implying an effect of the virus on the ion transport in these tissues. In the present study the physiological consequences of RSV infection were investigated in a cell culture model using the H441 human bronchial epithelial cell line. Cells were gown to confluent monolayers on semi-permeable filters in the presence of dexamethasone. Initial studies have shown that in this configuration, the H441 cell line develop a Na+ absorbing phenotype. Cells are then infected, at a multiplicity of infection of four, with either a live or UV?inactivated RSV strain. The UV??inactivated strain is capable of binding to and entering cells, but is unable to undergo viral replication. Viral infection was confirmed though confocal microscopy. 24 hours post infection, a statistically significant decrease in total current was observed for both strains; live 12.6 ± 3.1 to 5.2 ± 3.1 mA/cm2 (p < 0.02), UV- inactivated 13.4 ± 4.3 to 7.0 ± 2.7 mA/cm2 (p < 0.05), with no statistically significant change in control (11.0 ± 2.2 to 11.8 ± 2.0 mA/cm2, p > 0.05). These results suggest that RSV infection (though a live or UV-inactivated strain) inhibits Na+ transport in the H441 cell line within 24 hours post infection.