Martina Schroeder

The Host-Pathogen interaction lab is interested in the recognition of pathogens by the innate immune system, as well as strategies employed by pathogens to evade recognition or to manipulate the ensuing immune response for its own benefit. Viral recognition by the innate immune system is mainly mediated by two classes of pattern recognition receptors: endosomal Toll-like receptors (TLRs) and cytoplasmic RIG-like helicases (RLHs). Both classes detect viral nucleic acids and lead to the induction of type I interferons, which are potent anti-viral mediators. Signalling pathways connecting the anti-viral PRRs to transcription factor activation and interferon induction are beginning to be elucidated, and the lab hopes to contribute to their understanding. A lot of viruses have developed sophisticated mechanism to evade detection by PRRs and/or to actively inhibit the resulting signalling pathways in order to prevent transcription factor activation and the induction of pro-inflammatory and anti-viral mediators. Viral strategies for immune evasion or subversion are optimised during evolution; therefore they tend to target key aspects of the host anti-viral response. Studying the modulation of the host protein by the virus can provide information for the design of anti-viral therapeutics and give us an edge in the evolutionary battle against the virus. Current work in the lab focuses on the human protein DDX3, as three different viruses that pose major global health threats, poxviruses, HIV and HCV, have been shown to manipulate DDX3 function. HIV and HCV seem to require DDX3 for their replication, and it has therefore been proposed as a potential drug target. However, we have recently identified an anti-viral role for DDX3 in type I interferon induction; and DDX3 is also involved in cell growth control. Therefore, we believe that DDX3 function needs to be investigated in more detail before informed strategies for its therapeutic manipulation can be designed.