Abstract
The endothelium maintains a vascular barrier by controlling platelet and immune cell interactions, capillary tone and interendothelial cell (EC) adherence. Here we suggest common elements in play during viral infection of the endothelium that alter normal EC functions and contribute to lethal hemorrhagic or edematous diseases. In viral reservoir hosts, infection of capillaries and lymphatic vessels may direct immunotolerance without disease, but in the absence of these cognate interactions they direct the delayed onset of human disease characterized by thrombocytopenia and vascular leakage in a severe endothelial dysfunction syndrome. Here we present insight into EC controls of hemostasis, immune response and capillary permeability that are altered by viral infection of the endothelium.
Highlights
The endothelium maintains a vascular barrier by controlling platelet and immune cell interactions, capillary tone and interendothelial cell (EC) adherence
Similar patient cytokine responses are observed during dengue fever (DF), that occurs in the absence of hemorrhage or edema, and in patients that develop dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS; Halstead, 2002, 2008)
The likely ability of AV, Ebola virus (EBOV), and HVs to persistently infect their hosts without disease and tolerize host immune responses provides a notable divergence between asymptomatic and pathogenic infections of the endothelium
Summary
The endothelium maintains a vascular barrier by controlling platelet and immune cell interactions, capillary tone and interendothelial cell (EC) adherence. ECs permit fluid and cellular efflux without leakage, yet respond to diverse signals from tissues and the circulation, and elicit responses that regulate platelets, complement and immune cell activation as well as capillary dilation and permeability (Luscher and Barton, 1997; Willoughby and Loscalzo, 2002; Orfanos et al, 2004; Aird, 2008; Dvorak, 2010).
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