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Complement has emerged as a likely driver of the immune response and end-organ damage in COVID-19. In patients with severe disease, deposition of terminal complement and microthrombosis have been observed… Click to show full abstract
Complement has emerged as a likely driver of the immune response and end-organ damage in COVID-19. In patients with severe disease, deposition of terminal complement and microthrombosis have been observed in the lung, skin, kidney, and heart. Recently, we demonstrated that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein leads to amplification of the alternative pathway of complement on cell surfaces through competition with complement factor H (CFH) for binding heparan sulfate. Thus, in vitro, the SARS-CoV2 spike protein can convert an inactivator surface to an activator surface on nucleated cells.
Journal Title: Blood
Year Published: 2021
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