Virus interactions with endothelial cell receptors: implications for viral pathogenesis

被引:51
作者
Dalrymple, Nadine A. [1 ]
Mackow, Erich R. [2 ]
机构
[1] SUNY Stony Brook, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA
基金
美国国家卫生研究院;
关键词
HANTAVIRUS PULMONARY SYNDROME; NONSTRUCTURAL PROTEIN NS1; GROWTH-FACTOR PRODUCTION; DENGUE VIRUS; VASCULAR-PERMEABILITY; SPHINGOSINE; 1-PHOSPHATE; ENVELOPE PROTEIN; ANDES VIRUS; MICROVASCULAR HYPERPERMEABILITY; ADHERENS JUNCTIONS;
D O I
10.1016/j.coviro.2014.06.006
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The endothelial lining of the vasculature performs a vital role in maintaining fluid barrier functions despite balancing nutrient and fluid content of tissues, repairing localized damage, coordinating responses of a plethora of factors, immune cells and platelets through a multitude of endothelial cell surface receptors. Viruses that nonlytically cause lethal hemorrhagic or edematous diseases engage receptors on vascular and lymphatic endothelial cells, altering normal cellular responses that control capillary leakage and fluid clearance functions with lethal consequences. Recent studies indicate that receptors directing dengue virus and hantavirus infection of the endothelium contribute to the dysregulation of normal endothelial cell signaling responses that control capillary permeability and immune responses that contribute to pathogenesis. Here we present recent studies of virally altered endothelial functions that provide new insight into targeting barrier functions of the endothelium as a potential therapeutic approach.
引用
收藏
页码:134 / 140
页数:7
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