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Table 1 Potential mechanisms to explain how viral infections may predispose the host to develop fibrosis

From: Viruses as co-factors for the initiation or exacerbation of lung 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