Invading a host's red blood cells via the complement-complement receptor pathway has garnered considerable attention as a viral infection route. According to clinical and experimental evidence, complement is implicated in both intrahepatic and extrahepatic manifestations of chronic hepatitis C virus (HCV) infection . Direct Binding of the Complement Component C1q to Coinfected Cells with Human Immunodeficiency Virus (HIV) and Human T Lymphotrophic Virus-I (HTLV-I) . In vitro and in vivo, C1q inhibits antibody-dependent enhancement (ADE) of flavivirus infection in a subclass-specific manner . However, the Ebola virus (EBOV) uses the complement component C1q to enhance infection via antibody . The Ebola virus (EBOV)-antibody-C1q complex is cross-linked with the C1q receptor on the cell surface, increasing the virus's ability to enter the cell . The spectrum of human C1q is identical to that of the ZIKV E protein . It is, however, distinct from the E protein produced by the West Nile virus . Dengue virus infection and transcription of inflammatory molecules in THP-1 cells are decreased when C1q binds to the dengue virus . Symptoms of an activated complement system include paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and catastrophic antiphospholipid syndrome in patients with COVID-19 . The alternative approach plays a critical role. The classical complement pathway is activated before the onset of pneumonia during virus clearance . Complement activation contributes to systemic diseases associated with lung pathology and SARS-CoV infection . In comparison to mice lacking C4 or factor B, mice lacking C3 are more resistant to infection with SARS-CoV MA15 . This demonstrates that diseases caused by SARS-CoV involve multiple complement cascade components . The complement replacement pathway associated with severe COVID-19 is activated and amplified in patients with this more severe disease. It has been associated with markers of endothelial injury and hypercoagulability . The most severe COVID-19 patients experience cytokine storms, endothelial inflammation (endothelitis), and thrombosis due to the complement system being overactivated . However, patients treated with complement inhibitors recovered without experiencing any adverse effects .