As evidence suggests that the development of asthma may result in part from respiratory viral infection during infancy, which has a predilection for infecting, destroying and/or in some way biologically altering lower airway epithelium, this study will help to delineate whether the severity of that infection and other early-life events impact the risk of asthma and allergic disease development in later childhood. 3 Despite a high attack rate of developing asthma following viral bronchiolitis, the majority of children who have infant bronchiolitis do not develop childhood asthma. Thus while viral respiratory infections may alter lung physiology and target the inflammatory response to the lower airway, this may only occur during a vulnerable time period during development of the immune system or lung, or in the presence of other risk factors. This developmental component may further reflect important gene-environment interactions that regulate both short-and long-term airway physiological alterations that manifest themselves clinically as childhood asthma. Efforts to determine and define the role of these factors, including disease severity, maternal atopy and other environmental exposures, such as second-hand smoke, to asthma pathogenesis are the focus and goal of the TCRI.