Respiratory syncytial virus pneumonia:: mechanisms of inflammation and prolonged airway hyperresponsiveness

Purpose of Review Respiratory synctial virus is the leading pathogen associated with lower respiratory tract infection in young chuildren worldwide. The pathogenesis of acute bronchiolitis and the mechanisms by which the virus induces long term airway disease remain to be elucidated. This review highlights new findings reported in the English language medical literature from January 2004 to January 2005. Recent Findings Several studies have confirmed a strong association between respiratory synctial virus infection in infancy and an increased risk for recurrent wheezing. Evidence indicates that the exaggerated immune response and abnormal neurogenic mechanisms induced by the virus play a significant role in the pathogenesis of the disease. Different genetic and immune markers have been correlated with acute disease severity and with increased risk of long-term pulmonary abnormalities. Recently, the application of real time polymerase chain reaction has demonstrated the persistence of respiratory synctial virus RNA in the lungs of infected mice for months after innoculation. This unexpected observation has stimulated discussions as to whether the long term presence of the virus could contribute to the long-term airway disease observed in children after respiratory synctial virus lower respiratory tract infection. Summary Despite almost half a century of active research in to the pathogenesis of respiratory synctial virus-induced acute and chronic airway disease, many questions remain unresolved. Studies in animal models demonstrate that interventions reducing viral replication resulted in improvement of acute disease severity and long-term pulmonary abnormalities. The stage is ready for clinical studies to determine whether preventing or delaying the primary infection could reduce the incidence of recurrent wheezing in children.