When your wellness is affected by virus-induced asthma, even an innocuous respiratory infection, like the common cold, produced by rhinovirus, can have such devastating effects on your wellbeing. Treatment for this kind of asthma is difficult because wellness experts have so far had trouble distinguishing between virus-induced asthma, and that which is exacerbated by allergens, but now researchers have found a new way of doing exactly that.
For the study, which was published in the American Journal of Respiratory and Critical Care Medicine, Peter G. Gibson, M.B.B.S., of the John Hunter Hospital in New Lambton, Australia, along with seven associates, compared the sputum cellular profiles of 59 asthma patients who were experiencing an acute asthma exacerbation against those of 45 controls. This control group was made up of 14 people with stable asthma and no viral infection, 15 people with a viral infection but no asthma, and 16 uninfected, healthy people.
According to Dr Gibson, ‘A respiratory virus was detected in 46, or 78%, of the subjects with acute asthma.’ Specifically, the rhinovirus was detected in 83% of the cases, and influenza, enterovirus and respiratory syncytial virus were also present. The researchers also discovered that interleukin 1 (IL-10) is another major factor involved in the acute asthma exacerbations of the patients with respiratory infections.
‘IL-10 gene expression was significantly increased in acute asthma with virus infection when compared with virus infection controls, uninfected controls and subjects with stable asthma,’ Dr Gibson said. He went on to note that IL-10 gene expression, which broadly suppresses your immune responses, returned to normal levels when patients recovered from acute asthma. ‘Thus, IL-10 gene expression from airway cells appeared to be a feature of virus-induced acute asthma,’ he explained. As the researchers point out, other studies have found that viral infection increases your IL-10 protein levels in your nose and peripheral blood mononuclear cells.
After they described the gene expression and cellular profiles of these patients, the researchers concluded by saying that the results show that in virus-induced asthma, there are different mechanisms operating than those described in allergen-induced asthma.
According to an editorial on the article by William W. Busse, MD, and James E. Gern, MD, of the University of Wisconsin Hospital in Madison, the findings of the study are ‘a major step forward in identifying the key players in virus-provoked asthma’ but the team needs to place ‘host susceptibility factors, mechanisms of the acute and often unresponsive airflow obstruction, and effective treatment for both intervention and prevention’ in the puzzle, ‘to more fully understand how respiratory viruses induce an asthma exacerbation.’
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