Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/98985
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Type: Journal article
Title: Dengue virus-induced inflammation of the endothelium and the potential roles of sphingosine kinase-1 and microRNAs
Author: Aloia, A.
Abraham, A.
Bonder, C.
Pitson, S.
Carr, J.
Citation: Mediators of Inflammation, 2015; 2015:509306-1-509306-13
Publisher: Hindawi Publishing Corporation
Issue Date: 2015
ISSN: 0962-9351
1466-1861
Statement of
Responsibility: 
Amanda L. Aloia, Alexander M. Abraham, Claudine S. Bonder, Stuart M. Pitson and Jillian M. Carr
Abstract: One of the main pathogenic effects of severe dengue virus (DENV) infection is a vascular leak syndrome. There are no available antivirals or specific DENV treatments and without hospital support severe DENV infection can be life-threatening. The cause of the vascular leakage is permeability changes in the endothelial cells lining the vasculature that are brought about by elevated vasoactive cytokine and chemokines induced following DENV infection. The source of these altered cytokine and chemokines is traditionally believed to be from DENV-infected cells such as monocyte/macrophages and dendritic cells. Herein we discuss the evidence for the endothelium as an additional contributor to inflammatory and innate responses during DENV infection which may affect endothelial cell function, in particular the ability to maintain vascular integrity. Furthermore, we hypothesise roles for two factors, sphingosine kinase-1 and microRNAs (miRNAs), with a focus on several candidate miRNAs, which are known to control normal vascular function and inflammatory responses. Both of these factors may be potential therapeutic targets to regulate inflammation of the endothelium during DENV infection.
Keywords: Endothelium, Vascular; Humans; Dengue; Inflammation; Phosphotransferases (Alcohol Group Acceptor); MicroRNAs; Capillary Permeability
Description: Review article
Rights: © 2015 Amanda L. Aloia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
RMID: 0030041684
DOI: 10.1155/2015/509306
Appears in Collections:Molecular and Biomedical Science publications

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