Abstract
It is well known that RSV is the most frequent cause of bronchiolitis and pneumonia in infants requiring hospitalization worldwide. Also, RSV is the major etiologic agent of epidemic wheezing in infants. It has been suggested that severe RSV infection in infants might lead to the development of recurrent wheezing and/or bronchial asthma. Sigurs et al. reported that the relationship between severe RSV bronchiolitis in infancy and later development of asthma and allergy sensitization is still observed in children aged up to 18 years.
It has been speculated that there are two pathways by which RSV infection induces childhood asthma: (1) a direct effect on airways, and (2) an indirect effect on the immune system. In natural infections, airway epithelial cells are the primary sites for RSV invasion, and RSV replication induces cytokine/chemokine gene expression networks in a coordinated manner. Airway damage/remodeling continues over a prolonged period, because airways are still immature in infants. Also, RSV infection affects the immune system by acting on lymphocytes, which may indirectly induce allergic asthma.
Most infants with so-called asthma might have had recurrent viral wheeze. One of the most consistent findings in clinical studies of asthma is that allergy and viral infections synergistically increase the risk of acute exacerbations. Interestingly, it has been suggested that there are several phenotypes of early childhood recurrent wheezing disease. Clearer phenotype definitions both of early childhood viral disease and of subsequent recurrent wheezing disorders are required.
