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Raised prevalence of allergic respiratory diseases observed in the last 20 years seems to be associated with changes of environment and lifestyle, which favor a delayed acquisition of Th1 function in childhood. The purpose of this study is to review recent knowledge concerning the developing human immune system and its interaction with external environmental factors for a better understanding of the changing faces of allergic diseases through infancy and childhood in the allergy-prone individual.

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Recent studies in volunteers have demonstrated that the presence of local secretory IgA antibody against parainfluenza type 1 virus is more important than serum antibody in protection against subsequent homotypic virus infections ( 1, 2 ) . I t seems reasonable that this would be the case with other paramyxoviruses whose site of entry, replication and pathologic expression is limited similarly to the respiratory tract. Because of the importance of respiratory syncytial (RS) virus infection in infants and children, the nasal secretory antibody response was studied in 17 infants and children whose illness was due to naturally occurring RS virus infection. The findings, presented here, have implications for immune prophylaxis and for understanding the pathogenesis of RS virus illness in infants and children.Materials and Methods: Serum and nasal secretions were obtained from infants and children in whom there was reasonable clinical suspicion that their illness might have been due to RS virus infection. Specimens were obtained at the time of admission to the hospital and approximately 3 weeks thereafter. Findings are reported only for those in whom RS virus infection was proven by virus recovery and/or a fourfold or greater rise in serum complement fixing (CF) antibody following illness. The nasal secretions were collected by gentle suction from the nostril following the periodic instillation of small amounts of 0.15 M saline solution. None of the secretions tested was grossly contaminated with blood. Secretions were stored a t *