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.