Respiratory syncytial virus (RSV) bronchiolitis is a major cause of childhood morbidity and mortality. Most infants are infected with respiratory syncytial virus in the first year of life, but a minority develop bronchiolitis for reasons unknown. The primary aim of this thesis was to determine the importance of type 1 and type 2 immunity in determining the outcome of RSV infection during infancy. Previous studies have established that antigen-specific priming of foetal T-cells can occur in utero from 22 weeks gestation. An additional aim of this thesis was to study the potential occurrence of prenatal sensitisation to RSV and it's immunological consequences. This thesis also sought to establish the relative incidence of respiratory pathogen infection during infancy. It is concluded that: (a) immune priming to RSV can occur antenatally if the mother is exposed at the appropriate stage of gestation and that this exposure is associated with a type 1 response, and (b) RSV bronchiolitis is associated with a marked imbalance in type 1/type 2 cytokines in favour of a type 2 response. These data combined suggest that priming of foetal T cells to RSV may result in a reduced severity of subsequent RSV disease by augmenting the infant's own type 1 specific cellular immune response to RSV. This may explain much of the clinical diversity of RSV disease and raises the possibility that RSV infection/immunisation of mothers after 22 weeks gestation might represent a new strategy for prevention of RSV bronchiolitis.