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Innate immunity in paediatric viral wheezers is virus specific and not interferon dependent
  1. Sejal Saglani
  1. Correspondence to Dr Sejal Saglani, Leukocyte Biology and Respiratory Paediatrics, National Heart & Lung Institute, Imperial College London, 368 Sir Alexander Fleming Building, Exhibition Road, London SW7 2AZ, UK; s.saglani{at}

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Up to a third of all children develop virus induced wheezing, but we still do not understand why some children wheeze with viral colds and others do not. We also do not know why only some viral wheezers progress to develop asthma and others do not. Data from the Childhood Origins of Asthma Study (COAST) have shown that children with at least one atopic parent who wheeze with viral infections in the first 3 years of life have a significantly increased risk of developing asthma.1 Specifically, wheezing with human rhinovirus (HRV) in the third year of life was associated with up to 30-fold higher risk. However, this association did not delineate whether virus infection caused asthma, or underlying susceptibility to asthma or early sensitisation resulted in altered immune responses to viral infections which subsequently resulted in an asthma phenotype. We now know that an underlying susceptibility is an important determinant since variants at the 17q21 locus were associated with asthma in children who had had HRV wheezing illnesses in COAST and another unrelated high risk birth cohort.2 Moreover, allergic sensitisation precedes HRV induced wheezing and asthma development.3 However, we still know very little about the nature of the immune responses to viral infection in susceptible children who may go on to develop asthma compared with those who are likely to outgrow their symptoms. A consequence of our limited understanding of the mechanisms underlying virus associated wheezing is that currently therapeutic options remain limited …

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  • Competing interests None.

  • Provenance and peer review Commissioned; internally peer reviewed.

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