On the other hand, the role of “virome” as a pro-fibrotic mediator has been further dissected in the context of aged-related development of lung fibrosis by demonstrating that only aged mice (>15 months) develop γ-herpesvirus-68-induced lung fibrosis through a mechanism that involved alveolar epithelial cell reprogramming to produce pro-fibrotic factors and enhanced TGF-β signaling in lung fibroblasts (68). This evidence concerns the gene TGFB1 and pulmonary fibrosis.