Respiratory syncytial virus (RSV) infection in early childhood is a risk factor for the development of wheezing, significant decreases in pulmonary function and increases in airway reactivity. Respiratory syncytial virus infection also exacerbates recurrent wheezing attacks in patients with established asthma. Here we review the present understanding of RSV-induced bronchial asthma, especially concerning the role of eosinophils. Recent evidence suggests that eosinophils are important in RSV infection and RSV-induced asthma. For example, the eosinophil count and concentrations of eosinophil cationic protein, an eosinophil toxic granule protein, were elevated in samples of blood and nasopharyngeal secretions from patients with RSV infection or RSV-induced asthma; this suggests that eosinophils degranulate in the respiratory tract during RSV infection. Respiratory syncytial virus can infect human eosinophils, which produce chemokines such as RANTES, monocyte chemotactic protein-1 and macrophage inflammatory protein-1α. We have demonstrated that RSV enhances superoxide production by human eosinophils stimulated with a lipid mediator, such as platelet-activating factor. This response is dependent on β2 integrin, αMβ2, which is critical for eosinophil effector functions. Previous studies have demonstrated that RSV-infected epithelial cells produce multiple cytokines and chemokines. We have found that RSV enhances eosinophil adhesion and degranulation following infection of BEAS-2B bronchial epithelial cells and that another eosinophil toxic granule protein, major basic protein or eosinophil peroxidase, synergistically augments RSV-induced epithelial cell damage and apoptosis in A549 cells. These results suggest that eosinophils and their products enhance RSV-induced airway inflammation in asthma. Closely delineating the mechanism by which RSV enhances eosinophilic inflammation in asthma should be useful in devising more effective therapy.