Most work on the pathogenesis of asthma has loss of ciliated and non-ciliated cells from the tracheal epithelium and the basal epithelial studied airway inflammation using allergen challenge as a model. 1 Although appropriate layer remaining intact. Regeneration of the epithelial layer began at five days and was complete for our understanding of the underlying disease pathology, epidemiological studies have sug-by two weeks. Studies of chickens infected with viral laryngotracheitis18 and guinea pigs gested that allergens are not common precipitants of asthma attacks2 3 and cohort studies infected with parainfluenza 3 virus19 have demonstrated that virus induced epithelial dishave demonstrated the importance of upper respiratory tract (URT) viruses as probably the ruption leads to significant increases in epithelial permeability and, as a consequence, commonest cause of asthma exacerbations. 4 5 Studying the effects of URT viruses should an increase in permeability to allergens and an increase in allergen sensitisation. 19 Other therefore help our understanding of the mechanisms underlying exacerbations of asthma and workers have studied in some detail the effects of parainfluenza type 1 (Sendai) virus infection open up new avenues for therapeutic intervention. 6 In this review we shall consider some in the rat. 20 21 In this model viral infection also leads to significant morphological changes to of the effects of URT viral infection that are pertinent to their involvement in asthma and theairwayswiththeearlydevelopmentofmultifocal necrosis and sloughing of the epithelium speculate on possible mechanisms of virus induced asthma exacerbations. lining the bronchi and bronchioles. Work in humans has also demonstrated an effect of URT viruses on the epithelial integrity of the airways. In one study22 bronchoscopy