Untersuchung antiviraler Effektormechanismen und der Masernvirus-Ausbreitung in humanen Endothelzellen

麻疹病毒(MV)的内皮细胞亲和性在急性麻疹及其感染后并发症的发病机制中起重要作用。感染的内皮细胞可能在病毒引起的白细胞减少中起决定性作用，参与急性感染后麻疹脑炎，并可能支持MV进入中枢。在急性出血性麻疹或中枢神经系统并发症中，内皮细胞改变的临床表现的分子基础是广泛未知的。我们想要分析各种MV毒株和重组病毒在脐静脉和脑内皮细胞中的复制以及病毒的定向释放。在感染弱毒株和强毒株后，将研究内皮细胞的功能，如细胞因子和黏附分子的表达，以及通透性。这项研究的目的是确定可能导致抑制或增强感染的因素(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有什么后果。

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.