Untersuchung antiviraler Effektormechanismen und der Masernvirus-Ausbreitung in humanen Endothelzellen

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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.