Host epithelial–viral interactions as cause and cure for asthma

Research on the pathogenesis of asthma has concentrated on initial stimuli, genetic susceptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cells and smooth muscle) as critical steps leading to disease. Recent evidence indicates that the innate immune cell response to respiratory viruses also contributes to the development of inflammatory airway disease. We further develop this concept by raising the issue that the interaction between host airway epithelial cells and respiratory viruses is another aspect of innate immunity that is also a critical determinant of asthma. We also introduce a rationale for how antiviral performance at the epithelial cell level might be improved to prevent acute infectious illness and chronic inflammatory disease caused by respiratory viruses.

► Placing antiviral defense in the context of innate mucosal immunity. ► Understanding how a defect in antiviral defense causes asthma. ► Identifying the precise defect in antiviral defense in asthma. ► Devising a strategy to improve antiviral defense.