The battle between viral infection and antiviral immunity

Viruses and humans have coevolved for millions of years and during this time viruses have armed themselves with strategies to hijack or evade our first line of defense against infection - the innate immune system. In particular we are interested in understanding some of the immune evasion mechanisms used by viruses to target key cytosolic receptors of the innate immune system known as RIG-like receptors. RIG-like receptors can be likened to sentinels that specifically detect intracellular viral RNA from viruses such as hepatitis B, hepatitis C, respiratory syncytial virus and influenza A as the presence of viral RNA within the cell is indicative of an infection. Upon detecting viral RNA the RIG-like receptors trigger a signaling cascade that results in the production of antiviral mediators, NFκB and type I interferons. Viruses on the other hand can block, degrade, mimic and cleave specific proteins in the signaling cascade to replicate and persist in the host. Our ultimate aim is to understand the role of host proteins in antiviral immunity and how viral proteins unravel, evade or repurpose their function.