Lung cells from asthma sufferers fail to invoke critical anti-viral defenses when infected with the common cold virus, according to a study in the March 21 issue of The Journal of Experimental Medicine. These results could help explain why respiratory viral infections are often more severe in people with asthma and how infection can trigger asthma attacks.

Past studies have shown that viruses can replicate themselves more extensively in the lungs of asthma sufferers than in healthy lungs. In this study, Wark and colleagues infected lung cell cultures with the common cold virus and found that the cells from asthma sufferers produced more virus than did those from healthy controls. The reason for this was twofold: the cells from asthmatics failed to produce the potent anti-viral protein interferon-beta (IFN-beta and also failed to initiate their own death--mechanisms used by healthy cells to limit virus replication and eliminate infected cells. These defects may be linked, as IFN-beta was recently shown to induce cell death in virus-infected cells.

How might this enhanced viral replication lead to asthma? The authors show that the cells from asthma sufferers, although unable to produce IFN-beta, could still secrete pro-inflammatory molecules, that can recruit asthma-inducing cells into the lungs. Future experiments are planned to identify the causes the IFN-beta defect. Although several genetic mutations have been linked to asthma in the past, so far none are related to IFNs.

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Contact: Nickey Henry
henryn@rockefeller.edu
212-327-8366
Journal of Experimental Medicine
21-Mar-2005

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