Rhinovirus, genes may interact to increase the risk of childhood asthma

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1. There is an association between certain chromosome 17q21 genotypes and human rhinovirus wheezing infections in the development of childhood asthma during early life. 

2.  This increased risk was not observed in those with the same genetic susceptibility (specific 17q21 genotypes) and non-wheezing human rhinovirus as well as any respiratory syncytial virus infections (non-wheezing and wheezing).

The pathogenesis of asthma involves a complex interaction between genetic factors as well as environmental exposures. Previous studies have demonstrated that those with certain genetic variations at chromosome 17q21 more susceptible to childhood-onset asthma. Certain viruses such as the human rhinovirus (HRV) and respiratory syncytial virus (RSV) have also been associated with both wheezing illness and subsequent development of asthma. This study reinforces the belief that asthma develops in the setting of a complex interplay between genetic and environmental susceptibilities.

The major limitation is the nature of the study in establishing causality – the effect of HRV wheezing illness in asthma may have been just one of many other predisposing factors. There was also a significant drop in the number of participants consenting to this study from the previous two cohorts (COAST and COPSAC), therefore it may have been underpowered and missed detecting interaction between asthma and RSV (type II error). Future studies will need to examine the complex mechanisms between genetic and environmental risk factors in the development of asthma.

Click to read the study in NEJM

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Image: PD

1. There is an association between certain chromosome 17q21 genotypes and human rhinovirus wheezing infections in the development of childhood asthma during early life. 

2. Similar associations were not identified for those who developed non-wheezing HRV infections and any respiratory syncytial infections (both wheezing and non-wheezing).

This [retrospective cohort study] examined the association between specific chromosome 17q21 genotypes and human rhinovirus (HRV) and respiratory syncytial virus (RSV) illness in the development of asthma. Data was compiled from three groups: two children’s cohorts (COAST [n=214] and COPSAC [n=297]) and one group of adult volunteers. The adult volunteers (n=100 with 23 diagnosed asthmatics) were recruited to examine genotype-specific expression of 17q21 genes in unstimulated and HRV-stimulated peripheral blood mononuclear cells (PBMC). The association between the “TT” genotype at chromosome 17p21 and asthma was present in children with HRV wheezing illness (26.1, 95% CI 5.1-133.0 in the COAST cohort and 3.9, 95% CI 1.3-11.7 in the COPSAC cohort). However, the relative increases in two transcripts (GSDMB and ORMDL3) by HRV-stimulated cells did not appear to be associated with any chromosome 17q21 genotype.

In sum: The pathogenesis of asthma involves a complex interaction between genetic factors as well as environmental exposures. Previous studies have demonstrated that those with certain genetic variations at chromosome 17q21 more susceptible to childhood-onset asthma. Certain viruses such as the human rhinovirus (HRV) and respiratory syncytial virus (RSV) have also been associated with both wheezing illness and subsequent development of asthma. This study reinforces the belief that asthma develops in the setting of a complex interplay between genetic and environmental susceptibilities.

The major limitation is the nature of the study in establishing causality – the effect of HRV wheezing illness in asthma may have been just one of many other predisposing factors. There was also a significant drop in the number of participants consenting to this study from the previous two cohorts (COAST and COPSAC), therefore it may have been underpowered and missed detecting interaction between asthma and RSV (type II error). Future studies will need to examine the complex mechanisms between genetic and environmental risk factors in the development of asthma.

Click to read the study in NEJM 

By Jonathan Liu and Mitalee Patil

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