Abstract
Until relatively recently, our view of acute viral respiratory illnesses in early childhood was somewhat limited. We “understood” the following: children were exposed to respiratory viruses by exposure to other children; all children would be exposed to common respiratory viruses during the first year or two of life, with many infections remaining subclinical and the minority becoming severe enough to warrant medical attention or hospitalization; human rhinovirus (HRV) did not cause lower airway infections in children; and normal children did not “carry” viruses in their upper airway. We also “knew” that lungs were normally sterile and, unlike the upper airway, the gastrointestinal tract, and the skin, did not have a resident microbiome. With data collected from community-based birth cohort studies and advances in diagnostic techniques, we now understand that many of our earlier concepts were flawed. Systematic studies of respiratory infections in communitybased birth cohort studies, the Childhood Asthma Study from Perth, Australia1 and the Childhood Origins of Asthma study from Wisconsin, USA2 have changed a number of these previously held beliefs. Both studies collected nasal samples from children at times of acute respiratory infections as well as control samples collected when the children were well. These studies firmly established that HRV was responsible for a considerable number of acute lower respiratory illnesses in early life, including those associated with wheeze, and that HRV could be identified in nasal samples collected from approximately 20% of children when they were completely well.1 In addition, definitive proof has been provided that
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