Endothelial dysfunction in dengue virus pathology

Summary Dengue virus (DENV) is a leading cause of illness and death, mainly in the (sub)tropics, where it causes dengue fever and/or the more serious diseases dengue hemorrhagic fever and dengue shock syndrome that are associated with changes in vascular permeability. Despite extensive research, the...

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Published inReviews in medical virology Vol. 25; no. 1; pp. 50 - 67
Main Authors Vervaeke, Peter, Vermeire, Kurt, Liekens, Sandra
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.01.2015
Wiley Periodicals Inc
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Summary:Summary Dengue virus (DENV) is a leading cause of illness and death, mainly in the (sub)tropics, where it causes dengue fever and/or the more serious diseases dengue hemorrhagic fever and dengue shock syndrome that are associated with changes in vascular permeability. Despite extensive research, the pathogenesis of DENV is still poorly understood and, although endothelial cells represent the primary fluid barrier of the blood vessels, the extent to which these cells contribute to DENV pathology is still under debate. The primary target cells for DENV are dendritic cells and monocytes/macrophages that release various chemokines and cytokines upon infection, which can activate the endothelium and are thought to play a major role in DENV‐induced vascular permeability. However, recent studies indicate that DENV also replicates in endothelial cells and that DENV‐infected endothelial cells may directly contribute to viremia, immune activation, vascular permeability and immune targeting of the endothelium. Also, the viral non‐structural protein‐1 and antibodies directed against this secreted protein have been reported to be involved in endothelial cell dysfunction. This review provides an extensive overview of the effects of DENV infection on endothelial cell physiology and barrier function. Copyright © 2014 John Wiley & Sons, Ltd.
Bibliography:istex:0962E0213614F5ADFCEAB564A5EFFE40EB651C50
ArticleID:RMV1818
ark:/67375/WNG-RC43LK92-2
KU Leuven - No. PF no. 10/18 and GOA no. 15/019/TBA
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ISSN:1052-9276
1099-1654
DOI:10.1002/rmv.1818