SARS Coronavirus and Lung Fibrosis

Abstract

Severe acute respiratory syndrome (SARS) is an acute infectious disease with significant mortality. A novel coronavirus (SARS-CoV) has been shown to be the causative agent of SARS. The typical clinical feature associated with SARS is diffuse alveolar damage in lung, and lung fibrosis is evident in patients who died from this disease. The mechanisms by which SARS-CoV infection causes lung fibrosis are not fully understood, but transforming growth factor-β (TGF-β) and angiotensin-converting enzyme 2 (ACE2)-mediated lung fibrosis are among the most documented ones. The activation of the TGF-β/Smad pathway is critical to lung fibrosis. SARS-CoV infection not only enhances the expression of TGF-β, but also facilitates its signaling activity. The SARS-CoV receptor ACE2 is a negative regulator of lung fibrosis, and SARS-CoV infection decreases ACE2 expression. Therefore, SARS-CoV infection may lead to lung fibrosis through multiple signaling pathways and TGF-β activation is one of the major contributors.