Table 1.

Potential mechanisms to explain how viral infections may predispose the host to develop fibrosis

Lytic infections may kill lung epithelial cells

Latent infections may alter the phenotype (proliferation, apoptosis or mediator secretion) of various lung cells (for example, epithelial and mesenchymal cells)

Persistent viruses may provide repeated insults with reactivation

Infection may increase the production of pro-fibrotic mediators (for example, TGF-β) or diminish the production of anti-fibrotic mediators

Induction of epithelial to mesenchymal transition

Induction of chemokines and fibrocyte recruitment

Surfactant abnormalities

Enhanced inflammation

Alteration of p53 function

Microvascular injury