Dengue virus type 2 modulates endothelial barrier function through CD73
UMass Chan AffiliationsDepartment of Medicine, Division of Infectious Diseases and Immunology
Amino Acids, Peptides, and Proteins
Immunology of Infectious Disease
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AbstractDengue hemorrhagic fever is characterized by a unique vascular leakage syndrome. The mechanisms of endothelial barrier dysfunction in dengue hemorrhagic fever are not well understood. We examined the modulation of endothelial barrier function in dengue virus type 2 (DENV2) infections using primary human umbilical vein endothelial cells. We demonstrated that the increase in endothelial barrier function within 72 hours after DENV2 infection is mediated by type I interferon-dependent CD73 up-regulation. After 72 hours, DENV2 slowed the recovery of endothelial barrier function in response to tumor necrosis factor-alpha or vascular endothelial growth factor. This phenomenon was likely caused by type I interferon receptor signaling inhibition and lower CD73 levels in DENV2-infected endothelial cells. Our findings suggest that during DENV2 infection, endothelial barrier homeostasis is maintained by a balance between pro-inflammatory and pro-angiogenic cytokines, and type I interferon-dependent CD73 expression and activity.
Chinmay Patkar, Kris Giaya, and Daniel H. Libraty. Dengue Virus Type 2 Modulates Endothelial Barrier Function through CD73. Am J Trop Med Hyg 2013 88:89-94. doi:10.4269/ajtmh.2012.12-0474. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/29906
RightsCopyright 2013 The American Society of Tropical Medicine and Hygiene. This is an Open Access article distributed under the terms of the American Society of Tropical Medicine and Hygiene's Re-use License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.