Pichinde virus induces microvascular endothelial cell permeability through the production of nitric oxide
Pichinde virus induces microvascular endothelial cell permeability through the production of nitric oxide
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DOI：
10.1186/1743-422x-6-162
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发表时间：
2009-10-08
期刊：
影响因子：
4.8
通讯作者：
Voss, Thomas G.
中科院分区：
文献类型：
--
作者：
Brocato, Rebecca L.;Voss, Thomas G.
本报告首次证实了皮钦德病毒（PIC）对人内皮细胞的感染。PIC感染诱导诱导型一氧化氮合酶基因的上调;以及可检测的一氧化氮（NO）的增加。PIC诱导内皮细胞单层的渗透性增加，这可以在所有测量的时间点与另外的一氧化氮合酶抑制剂被废除，表明NO在内皮屏障功能的改变中的作用。因为NO已经显示出对某些病毒的抗病毒活性，所以在添加NO合酶抑制剂后测量病毒滴度，并且发现在改变感染的EC中的病毒载量方面没有效果。NO合酶抑制对PIC感染诱导的活化半胱天冬酶水平也没有影响。总之，这些数据表明，由皮钦德病毒感染诱导的NO产生对内皮细胞单层通透性具有致病作用。
This report is the first to demonstrate infection of human endothelial cells by Pichinde virus (PIC). PIC infection induces an upregulation of the inducible nitric oxide synthase gene; as well as an increase in detectable nitric oxide (NO). PIC induces an increase in permeability in endothelial cell monolayers which can be abrogated at all measured timepoints with the addition of a nitric oxide synthase inhibitor, indicating a role for NO in the alteration of endothelial barrier function. Because NO has shown antiviral activity against some viruses, viral titer was measured after addition of the NO synthase inhibitor and found to have no effect in altering virus load in infected EC. The NO synthase inhibition also has no effect on levels of activated caspases induced by PIC infection. Taken together, these data indicate NO production induced by Pichinde virus infection has a pathogenic effect on endothelial cell monolayer permeability.