Novel pathways in the pathogenesis of respiratory syncytial virus disease

Respiratory syncytial virus (RSV) is a leading cause of severe respiratory infections in infants and children. Extensive research in past decades has expanded our knowledge regarding the specific mechanisms involved in the pa thogenesis of RSV bronchiolitis and subsequent chronic obstructive airway d isease. Studies of RSV infection are performed in humans, cell culture mode ls, and animal models, each with their own specific limitations. A recently developed murine model in which pulmonary dysfunction can be monitored and quantified appears to add a powerful tool for the study of specific pathog enic mechanisms of experimental RSV infections. Both immunologic and nonimm unologic factors have been implicated in the pathogenesis of RSV-induced di seases. Recently, a hypothesis that RSV bronchiolitis may be the result of production of Th2-type cytokines has become popular. There are, however, st udies in human infants with RSV as well as in RSV-infected mice that sugges t this theory is incorrect, or at least an oversimplification. There is com pelling evidence that cells producing interferon gamma may contribute to RS V-induced wheezing, possibly through induction of leukotriene release. Amon g the nonimmunologic factors, pulmonary surfactant has recently attracted a ttention, especially because of the therapeutic implications for infants wi th severe bronchiolitis. A better understanding of the pathogenesis of RSV- induced diseases will be of considerable help in developing specific therap eutic strategies and in Vaccine development. (C) 2000 Wiley-Liss. Inc.