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The role of viral respiratory infections in lactating infants and other children continues to generate controversy. The debate concerns the difference, or the apparent differences, in the natural history of wheezing. Viral infections frequently provoke wheezing episodes in non-asthmatic small children but in the majority of these the wheezing disappears without the child subsequently developing asthma. In some cases, however, the wheezing persists and in others the child has asthma. Both the role of viral infection and the mechanisms by which wheezing can be produced in a previously healthy child or exacerbated in asthmatic children are unknown. Several hypotheses have been put forward to explain the relationship between viral infections and persistent wheezing and asthma: 1. Altered immune response to various allergens, whether producing sensitization to these allergens or inhibiting tolerance response to airborne allergens. The number of such patients is increasing, among them those with bronchiolitis, asthma, positive skin tests and specific IgE antibodies. Although there is no unanimity on the matter, these patients also present elevated IL-4 levels and reduced IFN-gamma levels. 2. Induction of inflammation typical of allergic asthma. This occurs when the virus interacts with T lymphocytes; (the natural response to viral infection is Th0 and Th1 lymphocyte differentiation and release of IFN-gamma, which has antiviral properties. In children infected with respiratory syncytial virus Th2 lymphocyte differentiation is produced, which is characteristic of allergic reactions, to the detriment of Th1); epithelial cells (in these cells active viral infection activates nuclear transcription kappa-beta and nuclear IL-6 factor, producing the release of numerous pro-inflammatory cytokines and chemokines as well as expression of adhesion molecules); eosinophils (inducing variable eosinophilia which, to a certain degree, has predictive value for the persistence of wheezing) and other inflammatory cells such as neutrophils and macrophages. In the same context, during viral respiratory infection, the presence of mediators (leukotrienes, especially LTC4, histamine, prostaglandins and tryptase) are observed in respiratory secretions and a correlation between levels of specific IgE mediators can be observed. 3. Increased allergic inflammation--producing bronchial hyperreactivity, mediator release by the various inflammatory cells and neuropeptides from C-sensitive fibers, and even interfering with nitric oxide bronchodilators. In spite of all of the above, it seems that recurrent wheezing after childhood bronchiolitis is not exclusively the result of viral infection and that other factors also play a role in this disease.