The fastest responding branch of our immune defense is the interferon (IFN) system. As an immediate response to infection, cells synthesize and secrete alpha/beta IFNs. Uninfected cells throughout the organism sense the IFN molecules and activate a signal transduction chain which results in the synthesis of more than 300 different proteins.
A subset of these proteins is specialized for antiviral activity, inhibiting viral replication at the levels of genome replication, mRNA transcription or protein translation. Other IFN-induced factors interfere with cell proliferation or shape the specific immune response. Viruses, in turn, have evolved sophisticated escape mechanisms. Most – or probably all – viruses are able to either inhibit IFN synthesis, bind and inactivate secreted IFN molecules, block IFN-activated signaling, or disturb the action of IFN-induced antiviral proteins.
Highly virulent RNA viruses with comparably small genomes are ideal model systems for pathogenesis and host defense. In my group, we are studying (i) the viral structures triggering IFN production in infected cells and (ii) the factors and mechanism viruses employ to escape this powerful antiviral defense.
