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Asthma is the most prevalent chronic respiratory disease worldwide.1 While much progress has been made to understand the determinants of asthma, why a specific individual develops asthma is not entirely clear. Within this discussion, it should be noted that asthma is not a homogenous disease; that is to say, there are many (endo)types of asthma.2 In children, the most common pattern is a T2 exaggerated immune response with eosinophils, interleukin (IL)-4, IL-5 and IL-13 playing important roles. While clearly asthma is a complex disease, some of the noise in the literature surrounding the determinants of asthma is a result of disease definition. The presence of wheezing or reduced FEV1 may represent a number of endotypes of asthma or indeed non-asthma phenotypes.
With this caveat in mind, it is clear that viral infections and allergic sensitisation are key factors associated with a diagnosis of asthma.3 Numerous epidemiological and experimental studies have provided this link. A popular paradigm postulates that recurrent respiratory viral infections at critical time periods of immune and lung development in childhood and infancy coupled with allergic sensitisation are associated with the development of asthma.4 What is often questioned is the direction of this association; is a child with an underlying asthma phenotype more likely to experience viral infections and develop allergy? Or is an otherwise healthy child who happens to get viral infections subsequently pushed into an asthma phenotype? Like many ‘either–or’ questions, the answer is likely ‘yes’; that is, either possibility or neither may be operational in different situations. Indeed, given that asthma is so heterogeneous, it is logical that there may be many ways to reach this diagnosis.
In Thorax …
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