Our lab is interested in understanding how T cells respond to chronic antigen stimulation during persistent viral infections. To this end, our lab investigates cytomegalovirus (CMV), a ubiquitous herpesvirus that infects most people world-wide and persists for life. In healthy individuals CMV is continuously controlled by the immune system and causes little or no pathology. However, this constant control of CMV results in the slow accumulation of virus-specific T cells to extraordinary levels. On average, CMV-specific T cells comprise 4% to 5% of all T cells in infected individuals. These large numbers of CMV-specific T cells are thought to be vital for maintaining control of the infection and immunocompromised individuals can develop severe CMV-caused morbidity and mortality. However, the mechanisms by which these T cells are generated and maintained are not understood. Additionally, we don’t understand what effect these cells might have on the immune system as a whole. This may be particularly relevant during ageing as CMV-specific populations become increasingly dominant. Indeed, CMV infection has been linked to the development of an “Immune Risk Phenotype” that describes people who respond poorly to new infections or vaccines. To study CMV, we use murine cytomegalovirus (MCMV), a homologue of human CMV (HCMV) and a natural mouse pathogen. Like HCMV, infection of mice with MCMV results in the slow accumulation of functional, viral-specific T cells over time and it is this process that forms the foundation of our research interest. Currently we focus on two broad questions: 1) What are the mechanisms by which CMV-specific T cell are primed, accumulate and persist and 2) How does the presence of these population impact the overall generation and homeostasis of memory T cells specific for other infections.