A diagrammatic representation of the role of vWbp of S aureus in the initiation of vascular infections under physiological flow conditions. The underlying extracellular matrix of vascular tissue is exposed following damage to vascular endothelial cells. VWF released from these cells can then bind to collagen in the extracellular matrix and acts as a bridge to promote S aureus attachment to the damaged tissue via vWbp under shear stress. vWbp further enhances infected vascular lesions by promoting the attachment of platelets to the site of infection through its procoagulant role in staphylothrombin, converting soluble fibrinogen to fibrin and promoting the attachment of S aureus to platelets via clumping factor adhering to fibrin.