Potential Mechanisms Causing Delayed Effects of Respiratory Syncytial Virus Infection

Respiratory syncytial virus (RSV) and measles virus are both paramyxoviruses. Children who have been admitted to hospital with acute RSV bronchiolitis often suffer from recurrent wheezing in later childhood; much more rarely, measles causes a delayed central nervous system infection (e.g., subacute sclerosing panencephalitis [SSPE]) appearing up to 7 yr after the acute disease. Whether postmeasles SSPE is the equivalent of post-RSV wheezing has never been determined. The purpose of this review is to speculate regarding the causal or linked mechanisms that might be responsible for the association between severe infantile RSV infection and later respiratory symptoms. RSV bronchiolitis usually affects children less than 6 mo of age and has a peak incidence at 2 to 4 mo (1). During the postnatal period, the lungs are developing rapidly and undergoing alveolar septation. Bronchiolitis is the commonest severe insult to the lungs during this critical window and might cause long-term effects by delaying or preventing normal postnatal development. This may result in smaller lungs that are subsequently more susceptible to disease and infection. For measles, it is clear that persistent infection is the cause of SSPE; for RSV, it is not yet clear whether bronchiolitis is a marker of susceptibility to later wheezing disorders or itself causes delayed effects. This article reviews the immunobiology of RSV and some of the immunologic and virologic mechanisms that could explain the link between early infection and the subsequent development of respiratory disease.