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Tissue plasminogen activator induced by dengue virus infection of human endothelial cells
Author(s) -
Huang YingHuey,
Lei HuanYao,
Liu HsiaoSheng,
Lin YeeShin,
Chen ShunHua,
Liu ChingChuan,
Yeh TraiMing
Publication year - 2003
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10438
Subject(s) - dengue fever , dengue virus , virology , endothelial stem cell , plasminogen activator , pathogenesis , biology , hemostasis , antibody , umbilical vein , immunology , virus , tissue plasminogen activator , in vitro , medicine , endocrinology , biochemistry
Abstract Dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS) are severe complications of dengue virus (DV) infection. However, the pathogenesis of hemorrhage induced by dengue virus infection is poorly understood. Since endothelial cells play a pivotal role in the regulation of hemostasis, we studied the effect of DV infection on the production of tissue plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI‐1) in vitro using both primary isolated endothelial cells, human umbilical cord veins cells, and a human microvascular endothelial cell line. DV infection significantly induced the secretion of tPA but not PAI‐1 of human endothelial cells. In addition, tPA mRNA of endothelial cells was induced by DV as demonstrated by RT‐PCR. Antibody against IL‐6 but not control antibody inhibited DV‐induced tPA production of endothelial cells. Furthermore, a good correlation between sera levels of IL‐6 and tPA was found in DHF but not DF patients. These results suggest that IL‐6 can regulate DV‐induced tPA production of endothelial cells, which may play important roles in the pathogenic development of DHF/DSS. J. Med. Virol. 70:610–616, 2003. © 2003 Wiley‐Liss, Inc.