Untersuchung antiviraler Effektormechanismen und der Masernvirus-Ausbreitung in humanen Endothelzellen

抗病毒效应机制和麻疹病毒在人内皮细胞中传播的研究

• 批准号: 5389805
• 负责人: Professor Dr. Jürgen Schneider-Schaulies
• 金额: --
• 依托单位: Institut für Virologie und Immunbiologie
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2002
• 资助国家: 德国
• 起止时间: 2001-12-31 至 2008-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/5389805?language=en
• 关键词: Untersuchung; antiviraler; Effektormechanismen; und; der

The endothelial cell tropism of measles virus (MV) plays an important role for the pathogenesis of acute measles and complications following the infection. Infected endothelial cells may decisively contribute to the virally induced leukopenia, participate at the acute postinfectious measles encephalitis, and may support the entry of MV in the CNS. The molecular basis underlying clinical findings of endothelial alterations during acute and haemorrhagic measles, or CNS-complications are widely unknown. We want to analyse the replication of various MV-strains and recombinant viruses in, and the directed virus release from umbilical vein and brain endothelial cells. Following infection with attenuated and virulent MV-strains, endothelial cell functions such as the expression of cytokines and adhesion molecules, and the permeability will be investigated. The study aims to identify factors (cytokine milieu) which may lead to inhibition or enhancement of the infection, and which consequences this has for the transmigration of leukocytes through the endothelium and for the virally induced leukopenia.

麻疹病毒（MV）的内皮细胞嗜性在急性麻疹的发病机制及并发症中起重要作用。感染的内皮细胞可能决定性地导致病毒诱导的白细胞减少，参与急性感染后麻疹脑炎，并可能支持MV进入CNS。在急性和出血性麻疹或CNS并发症中，内皮细胞改变的分子基础尚不清楚。我们希望分析各种MV株和重组病毒在脐静脉和脑内皮细胞中的复制，以及定向病毒释放。在用减毒和毒性MV菌株感染后，将研究内皮细胞功能，例如细胞因子和粘附分子的表达以及渗透性。该研究旨在确定可能导致感染抑制或增强的因素（细胞因子环境），以及这对白细胞通过内皮的迁移和病毒诱导的白细胞减少症的影响。