Viral respiratory infections induce airway hyperresponsiveness in asthmatic patients, in healthy persons, and in a number of animal species. In asthmatics the degree of airway hyperresponsiveness is associated with the severity of exacerbations. The respiratory tract of an asthmatic is inflamed, and these inflammatory cells might be involved in modulating airway responsiveness. In contrast, no data are available on the role of bronchoalveolar cells in the airways of "healthy" persons or asthmatic patients suffering a respiratory tract infection. Because of the lack of information on this issue, the present review has been written. A number of animal studies have now been performed suggesting the involvement of inflammatory cells during a viral respiratory infection. The changes in number and activity of bronchoalveolar cells after a viral infection have been compared with changes in airway morphology and the development of airway hyperresponsiveness. Based on these data we suggested, the following hypothesis: Viruses damage the epithelial layer of the respiratory tract and activate bronchoalveolar cells. Subsequently, a number of mediators are released that can stimulate metachromatic cells, which in turn release products that increase vascular permeability and attract inflammatory cells that might cause additional epithelial damage. Finally, the released mediators and the morphologic changes together results in airway obstruction and the development of hyperresponsiveness.