We read with interest the paper by BERGAUER et al. [1] on innate immune responses to viral infection in paediatric asthma. The paper confirms previous reports on impaired interferon responses in stable asthma [2-4], but describes a hyperactive interferon production during asthma exacerbations associated with rhinovirus infection. The authors conclude that, despite impaired immune condition at stable state, the ability to upregulate type I interferons during the acute phase is preserved in asthmatic children. However, what is lacking from this study is the information on interferon production during acute rhinovirus infection in an age-matched group of non-asthmatics. Thus, how can it be conclusively excluded that the production of interferon is impaired during the rhinovirus-induced acute phase of asthma in the absence of such a comparative control group? A study which examined nasal washes of children during acute episodes of wheezing or rhinitis, reported lower levels of IFN-λ in children with wheezing than in those with acute rhinitis, even if the differences were not statistically significant [5]. The fact that asthmatic patients, once infected, have more severe manifestations of the infectious diseases [6] could possibly suggest an impaired response also in the acute phase, but conclusive data are lacking.

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We analysed the influence of rhinovirus (RV) in nasopharyngeal fluid (NPF) on type I and III interferon (IFN) responses (e.g. IFN-α and IFN -: λ) and their signal transduction, at baseline and during disease exacerbation, in cohorts of pre-school children with and without asthma.At the time of recruitment into the Europe-wide study PreDicta, and during symptoms, NPF was collected and the local RV colonisation was analysed. Peripheral blood mononuclear cells (PBMCs) were challenged in vitro with RV or not. RNA was analysed by quantitative real-time PCR and gene arrays. Serum was analysed with ELISA for IFNs and C-reactive protein.We found that PBMCs from asthmatic children infected in vitro with the RV1b serotype upregulated MYD88, IRF1, STAT1 and STAT2 mRNA, whereas MYD88, IRF1, STAT1 and IRF9 were predominantly induced in control children. Moreover, during symptomatic visits because of disease exacerbation associated with RV detection in NPF, IFN-α production was found increased, while IFN-λ secretion was already induced by RV in asthmatic children at baseline.During asthma exacerbations associated with RV, asthmatic children can induce IFN-α secretion, indicating a hyperactive immune response to repeated respiratory virus infection.