Fig. 4.

Pathogenesis of SARS-CoV, MERS-CoV, and SARS-CoV-2. SARS-CoV and SARS-CoV-2 play a pathogenic role by inhibiting ACE2. Under the influence of renin and ACE, angiotensinogen is converted into Ang II. Through the AT1 receptor, Ang II acts as a lung injury-promoting factor, and in some cases, may cause vascular constriction, an inflammatory response, cell proliferation, fibrosis, and apoptosis of alveolar epithelial cells, resulting in diseases such as pulmonary hypertension, pulmonary fibrosis, and acute lung injury. ACE2 converts Ang II into Ang (1–7), and through the MAS receptor, Ang (1–7) play roles in vasodilation, antiproliferative activity, and antioxidant activity. SARS-CoV downregulates the activity of ACE2 and causes an increase in the amount of Ang II and lung injury. MERS-CoV infection of dendritic cells and macrophages can lead to the continuous production of pro-inflammatory cytokines and chemokines, leading to a large number of immune cells infiltrating a patient’s lower respiratory tract, causing severe inflammation and tissue damage. MERS-CoV can infect T-cells from human lymphoid organs and causes the peripheral blood inducing apoptosis by intrinsic and extrinsic pathways, thus avoiding host immune response