In this issue, Culley et al.(1) present findings from an infant mouse model of respiratory syncitial virus (RSV) infection, which provides a new perspective on the pathogenesis of RSV-mediated lung disease in early life. RSV is one of the most common respiratory pathogens encountered in pediatric practice, and virtually all children experience one or more infectious episodes by the age of 2 yr (2). The initial focus of the infection is the nasopharyngeal epithelium, and in the majority of cases it remains localized to this area and the symptomatology is restricted to a runny nose. In a subset of subjects, however, the virus spreads to the lower respiratory tract, resulting in a wheezing illness or acute bronchiolitis that requires hospitalization. Between 50 and 90% of hospitalizations for bronchiolitis amongst children in the US are directly attributable to RSV and substantial increases have been documented recently in admissions in North America (2), paralleling the spiralling increase which is occurring in asthma in pediatric and adult populations throughout the developed world. A possible causal link between RSV-induced wheeze in infancy and later development of persistent asthma has been widely debated in this field, and elucidation of the factor (s) responsible for susceptibility to these apparently related diseases is considered a matter of urgent priority in pulmonary medicine. However, the precise nature of this linkage is increasingly controversial, as discussed below.