Figure 6.
Proposed model for SARS-CoV-2 induced APC activation. Under normal conditions, factor H binds to HS on the cell surface and interacts with C3b, which facilitates factor I cleavage and deactivation of C3b. Upon infection, SARS-CoV-2 spike protein binds to HS on the cell surface and interferes with factor H function, which facilitates factor B binding to C3b and cleavage by factor D. AT III, antithrombin III; CFH, factor H; ecSOD, extracellular superoxide dismutase; FGF2, fibroblast growth factor 2; HB-EGF, heparin-binding epidermal growth factor; TGF-β, transforming growth factor β; VEGF, vascular endothelial growth factor.

Proposed model for SARS-CoV-2 induced APC activation. Under normal conditions, factor H binds to HS on the cell surface and interacts with C3b, which facilitates factor I cleavage and deactivation of C3b. Upon infection, SARS-CoV-2 spike protein binds to HS on the cell surface and interferes with factor H function, which facilitates factor B binding to C3b and cleavage by factor D. AT III, antithrombin III; CFH, factor H; ecSOD, extracellular superoxide dismutase; FGF2, fibroblast growth factor 2; HB-EGF, heparin-binding epidermal growth factor; TGF-β, transforming growth factor β; VEGF, vascular endothelial growth factor.

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