Origins of reactive airways disease in early life: do viral infections play a role?

Abstract

There is mounting evidence suggesting that infection with respiratory syncytial virus (RSV) in early life increases the risk of developing reactive airway disease (RAD) later in childhood. A recent prospective study demonstrated that children hospitalized with RSV bronchiolitis in infancy face a significantly increased risk of recurrent wheezing and allergy at least until the age of 7 y that is independent of hereditary factors. Proposed mechanisms for this link include immune dysregulation, in which RSV-specific IgE or an imbalance between T-lymphocyte-dependent immune pathways may be involved, and abnormal neural control, in which the non-adrenergic, non-cholinergic pathways are altered by RSV infection. More recent studies suggest that immune and neural mechanisms may be linked and that post-RSV airway inflammation may be explained, at least in part, on the basis of these neuroimmune interactions. Passive immunoprophylaxis may protect against persistent viral-induced inflammation of the respiratory tract, long-term changes in pulmonary function and increased frequency of RAD episodes.