Abstract
Lower respiratory tract virus infections are the major cause of asthma exacerbations. Severity of infection and age at initial encounter with virus appear to be major determinants of the risk for allergic asthma later in life. In animal models, reinfection of mice initially infected as neonates leads to markedly enhanced alterations in airway function and inflammation, unlike reinfection of older mice. Both innate and adaptive immune responses contribute to this susceptibility with lung dendritic cells showing marked differences in phenotype and function in young compared to older mice, and these differences are further enhanced following virus infection. These findings have implications for therapeutic targeting, for example, of RSV G and F surface proteins at different stages of the response to infection.