Ebolaviruses are zoonotic pathogens causing severe hemorrhagic fevers in humans and non-human primates with high case fatality rates. In recent years, the number and scope of outbreaks has increased, highlighting the importance of better understanding the molecular aspects of ebolaviral infection and host cell interactions in order to be able to better control this virus. To facilitate virus genome replication, transcription and protein expression, ebolaviruses recruit and interact with specific host factors. These interactions play a key role in viral infection and influence virus survival and disease outcome. Based on a genome-wide siRNA screen, the three host factors CAD, NXF1 and UAP56 were recently identified to be involved in ebolavirus genome replication and/or transcription and/or mRNA-translation. However, mechanistical details of how these host factors affect the ebolavirus lifecycle remained elusive. In this thesis I analyzed the functional interactions between EBOV and these newly identified host proteins in order to better understand the virus-host interface. To this end I used siRNA knockdown as well as overexpression of these host proteins in combination with different reverse-genetics based lifecycle modelling assays to investigate the influence of CAD, NXF1 and UAP56 on individual aspects of the EBOV lifecycle. Using these systems in relation with a host factor knockdown I was able to show that the provision of pyrimidines by CAD plays an important role for ...