Dengue Virus Type 2 Modulates Endothelial Barrier Function Through CD73

Overview

Journal Am J Trop Med Hyg

Specialty Tropical Medicine

Date 2012 Nov 15

PMID 23149581

Citations 9

Authors

Chinmay Patkar

Kris Giaya

Daniel H Libraty

Affiliations

Soon will be listed here.

Abstract

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-α 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.

Citing Articles

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Purinergic modulation of the immune response to infections.

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