Effect of respiratory syncytial virus infection during early infancy on the ontogeny of cytokine immune responses.

Recently, childhood asthma has been associated with an alarming rise in prevalence, morbidity, and mortality. Strong epidemiological evidence now links the development of childhood asthma with the persistence of T-helper lymphocyte type 2 (Th2) cytokine immune responses during early infancy. However, the ontogeny of human cytokine immune responses and the environmental factors influencing their development have not been fully elucidated. Several lines of evidence support the hypothesis that respiratory syncytial virus (RSV) infection during early infancy induces/amplifies the persistence of Th2 cytokine immune responses. Moreover, results from recent studies suggest that diminished interleukin (IL)-12 production by dendritic cells (DCs) is a potential mechanism by which RSV infection predisposes to the persistence of Th2 cytokine responses. Studies are needed to characterize the ontogeny of DC IL-12 production and Th cytokine responses during early infancy and to investigate the effect of RSV infection during early infancy on these responses. Results from such research may provide insight into the mechanism by which RSV infection may predispose to the development of childhood asthma. Moreover, they may result in the identification of potential strategies to attenuate or prevent the development of RSV infection and/or childhood asthma. Such strategies may include administration of IL-12 or manipulation of DC maturation or function.