Respiratory viral infections are very important triggers of asthma exacerbation. Recent epidemiologic studies support the hypothesis that they are associated with 80 to 85 % of acute attacks of asthma in children, both in mild exacerbations, and in more severe exacerbations leading to hospital admission. The respiratory syncytial and parainfluenza viruses are predominantly detected in infants, while rhinovirus and mycoplasma are the commonest viruses in children. The detailed mechanism of virus-induced exacerbations remains poorly understood, al though recent studies have provided evidence of increased activation of inflammatory cells in bronchial lavage. Allergic individuals, outside of periods of allergy, do not seem to have more virus-induced respiratory manifestations than nonallergic individuals. In contrast, rhinovirus infection may intensify both the immediate and late response to allergen challenge by increasing mast cell mediator release and recruitment of eosinophils in the lower airways. Human and animal studies suggest that local production of cytokines (IL4, IL8, RANTES, MIP-1a...) and the increased expression of intercellular adhesion molecule 1 (ICAM1) in asthmatic individuals, may play an important role for recruitment and activation of inflammatory cells in the airways. One hypothesis, that remains to be demonstrated, would be that in the presence of Th2 predominance, as occurs in asthma, an excess of IL4 could inhibit the development of cytotoxic CD8, NK and Th1 activity, thereby resulting in decreased IFN production, more severe allergic inflammation and less efficient viral clearance.