Deficient immune response to viral infections in children predicts later Asthma persistence

Rhinovirus infection is the most frequent cause of asthma exacerbations in children, and respiratory viral infections in early life have been associated with increased risk for asthma later on (1). However, the mechanisms driving this association are incompletely understood. We recently showed that deficient antiviral immune responses by bronchial epithelium, with decreased rhinovirus-induced IFN production and increased viral replication, are already present in preschool children with asthma (with or without atopy) and in atopic children without asthma (2). Our original cohort of 34 children was prospectively followed for 8 years to investigate whether the impaired rhinovirus- induced IFN production seen in the original population could be a risk factor for the development of asthma later in life (as diagnosed by a respiratory pediatrician blinded to antiviral response data). Our results seem to confirm this possibility. Analyses of epithelial IFN production and viral replication along with epithelial destruction and eosinophil counts in bronchial biopsies were performed as previously reported (2). Follow-up data were available for 27 children: 62% of children with asthma at baseline remained asthmatic at follow-up, whereas 21% of children with no asthma at baseline developed asthma.