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Details

Autor(en) / Beteiligte
Titel
Dengue virus infection of human microvascular endothelial cells from different vascular beds promotes both common and specific functional changes
Ist Teil von
  • Journal of medical virology, 2006-02, Vol.78 (2), p.229-242
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2006
Link zum Volltext
Quelle
Wiley Blackwell Single Titles
Beschreibungen/Notizen
  • Dengue shock syndrome (DSS), the major life threatening outcome of severe dengue disease, which occurs in some patients in the course of dengue infection, is the consequence of plasma leakage in the microvascular territories. Data from clinical and in vitro studies suggest that an inadequate immunological response is partly responsible for the pathophysiology of DSS, but few is known concerning the consequences of direct infection of endothelial cells by dengue virus per se. In this study, an attempt was made to study the response of two microvascular human cell lines originating, respectively, from liver and dermis to infection by a dengue type 2 virus, by analyzing the virus‐induced modulation of functional markers. It is shown that the two microvascular cell lines exhibit both common and specific behaviors upon infection. In particular, LSEC and HMEC‐1 replicate efficiently the low‐passage virus and respond to infection by over‐producing inflammatory mediators involved in the cross talk with circulating immune cells. However, direct infection modulates differently the cell surface expression of molecules critically involved in the interactions between endothelial and inflammatory cells. ICAM‐1 and HLA‐I are up regulated as a consequence of infection in LSEC whereas direct infection results in downregulation of ICAM‐1 in HMEC‐1. The present results show that infection of human microvascular cells by unadapted dengue virus results in both common and specific activation patterns depending likely on the tissue origin of the cells, thus suggesting that endothelia from different territories may contribute differently to the pathophysiological events in the course of dengue infection. J. Med. Virol. 78:229–242, 2006. © 2005 Wiley‐Liss, Inc.

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