Figure 1.

Mechanisms of virus-induced asthma exacerbations. In the normal airway epithelial cells, viral infection induces the production of IFN-β, which in turn induces apoptosis in virus-infected cells and limits virus replication. This is followed by an adaptive immune response characterized by Th1 cells that produce IFN-γ and IL-12, leading to a strong antiviral response, rapid clearance of the virus, and minimal inflammation. In asthmatic patients, both innate and adaptive antiviral immunity may be impaired, resulting in cell necrosis and the release of inflammatory mediators and virus. The increased viral load and levels of inflammatory mediators released from necrotic cells result in uncontrolled airway inflammation and exacerbation.