Endothelial cell dysfunction in viral hemorrhage and edema.

Front Microbiol

Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY, USA.

Published: January 2015

AI Article Synopsis

  • The endothelium plays a critical role in maintaining blood vessel integrity by regulating interactions between platelets and immune cells, as well as controlling capillary tone and the adherence of endothelial cells.
  • During viral infections, these normal endothelial functions can be disrupted, leading to serious conditions characterized by severe bleeding or swelling.
  • In some cases, while viral infections in certain hosts may lead to immunotolerance without immediate disease, they can eventually result in delayed human diseases marked by low platelet counts and increased vascular permeability, indicating severe endothelial dysfunction.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283606PMC
http://dx.doi.org/10.3389/fmicb.2014.00733DOI Listing

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