Furthermore, infection with γ-herpes virus-68 (γHV-68) increases the expression of TGF-β receptor 1 and activates TGF-β signaling in AEC2, leading to the increased phosphorylation of SMAD3 and enhanced apoptosis of AEC2 in mice with lung fibrosis, which ultimately results in the occurrence of AE [62]. Here, TGFB1 is linked to pulmonary fibrosis.