Respiratory virus infections often trigger asthma attacks, and these infections are more severe in asthma sufferers than in healthy individuals. Past studies have demonstrated increased virus replication in asthmatic versus healthy subjects and suggested that alterations in cytokine production that favor asthma-promoting T helper (Th)-2 responses might be to blame.

Wark and colleagues now uncover a defect that may provide the initial trigger for virus-induced asthma. They found that bronchial epithelial cells—the primary targets of viral infection—from asthma sufferers supported more virus replication than did cells from healthy controls. The reason for this was twofold: epithelial cells from asthmatic subjects failed to produce the potent anti-viral cytokine interferon-ß (IFN-ß) and also failed to initiate apoptosis, mechanisms employed by healthy cells to limit virus replication and eliminate infected cells. These defects may be linked, as IFN-ß was recently shown to induce apoptosis in virus-infected cells.

How does this enhanced viral replication lead to asthma? The authors show that epithelial cells from asthma sufferers, although unable to produce IFN-ß, could still secrete pro-inflammatory cytokines, which can recruit asthma-inducing eosinophils and Th2 cells to the lungs. Future experiments are planned to identify the mutation that causes the IFN-ß defect. Although several genetic markers have been linked to asthma in the past, so far none are related to IFNs.