Department of Medicine, Division of Infectious Diseases and Immunology
5'-Nucleotidase; Cells, Cultured; Dengue Virus; Endothelium, Vascular; Humans
Immunology of Infectious Disease | Infectious Disease | Virus Diseases
Dengue 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.
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Citation: 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
The American journal of tropical medicine and hygiene
Patkar, Chinmay; Giaya, Krisanthi; and Libraty, Daniel H., "Dengue virus type 2 modulates endothelial barrier function through CD73" (2013). University of Massachusetts Medical School Faculty Publications. 211.