The human immunodeficiency virus type 1 (HIV‑1) is characterized by a relatively small genome. It contains numerous cis-regulatory elements that enable precise regulation of the viral gene products. Since viral gene expression is dependent on the cellular machinery, efficient amounts of cellular regulatory proteins (so-called viral dependency factors) are of crucial importance for efficient virus replication. Among them, cellular RNA-binding proteins play a key role in HIV‑1 mRNA processing.
Interferons (IFNs) play an important role in innate immune defense against HIV‑1. They induce the transcription of IFN-stimulated genes (ISG) such as direct antiviral restriction factors, which create an antiviral state in the host cell. We have recently been able to show that after treatment with the clinically used IFNα2, the expression levels of certain RNA binding dependency factors are down-regulated in T cells and macrophages. Therefore, within the SPP1923 we investigate how interferons influence viral RNA processing and thus replicative capacity by removing important players of the viral replication cycle.