Dengue Virus neither Directly Mediates Hyperpermeability nor Enhances Tumor Necrosis Factor-α-Induced Permeability In Vitro

The mechanisms of endothelial barrier dysfunction in dengue disease remain poorly understood. Endothelial cell (EC) death due to virus infection or in combination with an infection-induced cytokine storm is deemed as one of the major causes of plasma leakage. Using an in vitro model of human endothelia and several dengue virus (DENV) strains (including a clinical isolate), the direct consequence of infection on endothelial permeability was investigated throughout the course of the infection. All employed DENV-2 strains were able to infect and replicate in ECs. Rather than increase endothelial permeability, DENV infection alone enhanced cell barrier integrity up to 7 days postinfection. Improved cell barrier function was mediated by type I interferon activation at the early phase of infection and by the survival advantage of the infected cells at the late phase of infection. Consistent with this phenomenon, DENV infection did not augment tumor necrosis factor-α-induced permeability. Our results prove that DENV infection does not directly account for vascular permeability; DENV neither induces hyperpermeability nor exacerbates the permeabilizing effect of cytokines. The contributory role of other factors on plasma leakage during dengue disease warrants further investigation.;開始ページ : 86;終了ページ : 94

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書名 Dengue Virus neither Directly Mediates Hyperpermeability nor Enhances Tumor Necrosis Factor-α-Induced Permeability In Vitro
著作者等 国立感染症研究所
Raekiansyah Muhareva
書名別名 デングウイルスの感染はそれのみで血管の透過性を亢進する作用はなくTNF-αの透過性亢進作用を増強することもない
出版元 国立感染症研究所
刊行年月 1999.2-2012.3
ページ数 v.
大きさ 30 cm
ISSN 13446304
NCID AA1132885X
AA12034049
※クリックでCiNii Booksを表示
全国書誌番号
10054631
※クリックで国立国会図書館サーチを表示
言語 英語
出版国 日本
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