Table 2.

Potential mechanisms for viral exacerbation of IPF

Th2 environment in fibrotic lungs may limit viral clearance

Epithelial cells in fibrotic lungs may be unable to effectively replace epithelial cells damaged by lytic infection

Increased chemokines may recruit and activate fibrocytes

Pro-inflammatory mediators secreted in response to infection may have pro-fibrotic effects

Steroid and immunosuppressive therapy may predispose the host for increased viral infection or reactivation

Microvascular injury