Fig. 1.

Overview of the role of complement inhibitors targeting complement cascade during SARS-CoV-2 infection. Upon infection, SARS-CoV-2 primarily affects the respiratory tract and alveolar cells of the lung through ACE receptors. Subsequently, SARS-CoV-2 directly interacts with MASP2 through a single N-linked glycosylation site in SARS-S and activates the MBL pathway. The classical and alternative pathways are also activated as a part of the viral defense, and triggers complement component C3, which culminates in increased secretion of C3a and C5a. These anaphylatoxins trigger cytokines storm, mast cells degranulation, activation of leukocytes and its infiltration into alveoli. The unsolicited activation of complement cascade starts here through DAMPs, and makes the lung vulnerable to complement deposits, excess neutrophil infiltration and pathogenesis of ARDS. Hence, inhibiting the downstream complement components such as C3 and C5, the convertases of C3 and C5, the anaphylatoxins C3a and C5a and its receptors will be a better approach to reduce the pathogenesis of ARDS. Inhibition of the above complement components would reduce the severity of the pathological conditions caused by the virus. Moreover, it will provide a window period for eliminating viral load with antiviral drugs for COVID-19 patients