FIGURE 4:

Hantavirus-caused pathogenesis is characterized by vascular leakage and platelet activation. Hantaviruses primarily infect endothelial cells, reducing their barrier function while increasing vascular permeability. Endothelial cell–cell contacts are disturbed by the downregulation of VE-cadherin in adherens junctions caused by vascular endothelial growth factor A (VEGFA) or bradykinin. Platelets are activated after hantavirus infection by either the direct interaction of viral glycoproteins and platelet integrin αIIβ3 or by endothelial cell damage releasing adhesive factors such as fibrinogen, fibronectin and von Willebrand factor. Hantavirus can additionally cause intravascular coagulation. Both activated platelets and coagulation contribute to thrombocytopenia. Source: Figure created with Biorender.com and figure concept adapted from Vaheri et al. [23].