Upon viral infection, type I IFNs induce the expression of hundreds of ISGs, thus establishing an antiviral state within host and bystander cells. Furthermore, IFNs also induce the repression of specific genes, termed IRepGs. Several of these IRepGs were identified as HDFs, which are essential for viral replication. HIV-1 exploits the cellular transcription and RNA processing machinery for viral replication. In particular, alternative splicing plays a crucial role in the viral life cycle and is regulated by a complex network of SREs, which are localized in the vicinity of viral splice sites and bound by cellular splicing factors. Members of the SRSF and hnRNP protein families were identified as HDFs and shown to regulate HIV-1 alternative splice site usage. This work aims to investigate, whether SRSF and hnRNP transcript levels are altered upon HIV-1 infection, possibly due to IFN induction and the concomitant inflammation. HIV-1 target cells will be stimulated with different IFNα subtypes to examine, whether the expression of specific SRSFs and hnRNPs is type I IFN-regulated. It will be evaluated, whether the potential modulation of SRSF1 and hnRNP A0 expression levels upon IFN stimulation might be a part of the type I IFN-induced antiviral activity. In addition, the effect of altered expression levels of SRSF1 and hnRNP A0 on HIV-1 post integration steps will be examined at the level of LTR transcription, alternative splicing and virus production. Thus, the importance of balanced levels of SRSF1 and hnRNP A0 for efficient HIV-1 replication will be investigated.