Lung function measurements in children - copsac
Lung function measurements in children - copsac
Lung function measurements in children - copsac
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viruses and early childhood asthma (42). In the light of these two particular papers Kuehni et<br />
al discussed the causal l<strong>in</strong>k between RSV <strong>in</strong>fection and asthma <strong>in</strong> an editorial (43). The<br />
editorial concluded the new data were more <strong>in</strong> favor of the hypothesis that the association<br />
between RSV and asthma is due to shared predisposition rather than to a causal effect of<br />
RSV. However, the authors po<strong>in</strong>ted out that the asthma phenotype was poorly def<strong>in</strong>ed <strong>in</strong> both<br />
studies.<br />
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A genetic contribution to asthma and severe RSV-bronchiolitis is suggested from the high<br />
prevalence of asthma <strong>in</strong> our tw<strong>in</strong> sample compared with the current asthma prevalence <strong>in</strong> our<br />
region (44-47) as well as the high prevalence of parental atopic predisposition <strong>in</strong> the present<br />
study. Likewise, such genetic component was reflected by our previous f<strong>in</strong>d<strong>in</strong>g of a higher<br />
concordance for hospitalization for RSV-bronchiolitis <strong>in</strong> MZ than DZ tw<strong>in</strong> pairs (28).<br />
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Several publications suggest that RSV <strong>in</strong>fection <strong>in</strong> early <strong>in</strong>fancy stimulates a Th2 response<br />
(48-53). Previous publications have found that severe RSV bronchiolitis was associated with<br />
genetic polymorphism (haplotype IL13-IL4) (54-57), which may play an important role <strong>in</strong> the<br />
Th2 response (skew). The same locus have been associated with atopy and asthma <strong>in</strong> other<br />
genetic studies (58-60). These studies together suggest that primary RSV bronchiolitis and<br />
atopy share a genetic contribution at the IL13-IL4 locus.<br />
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We found no differential effect from severity of RSV <strong>in</strong>fection on the asthma and allergy 7<br />
years after <strong>in</strong>fection. This may suggest that some undisclosed environmental factor <strong>in</strong>stead<br />
could be responsible for the different severities RSV <strong>in</strong>fection. The nature of such exposure is<br />
unknown and surpris<strong>in</strong>g <strong>in</strong> monozygotic tw<strong>in</strong>s. Studies suggest that phenotypic discordance<br />
between monozygotic tw<strong>in</strong>s is to some extent due to epigenetic factors. Acute environmental<br />
factors are directly associated with epigenetic-dependent disease phenotype (61-63).<br />
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