My laboratory investigates T cell immunity to viral infections. Our main interest is in herpesvirus immune evasion genes- how they function, and what effect this has on the immune response to the virus and the virus infective process. We use murine cytomegalovirus (MCMV) as our main model.
Cytomegalovirus (CMV) is a ubiquitous infection, infecting approximately 70% of adults in the US. CMV infects in childhood and establishes lifelong infection, usually without symptoms. Immunity to CMV occupies a surprisingly high proportion of the immune system throughout life: around 4% of CD4+ and 10% of CD8+ T cells in chronically infected people are specific for CMV, probably more than for any other virus. This high number of T cells is thought to be maintained by recurrent virus activity, which nevertheless normally remains below the threshold of detection. However, if immunity is compromised, CMV rapidly reactivates and is a main cause of morbidity in most clinically immunocompromized states. It thus appears that the chronic equilibrium between CMV and host involves a lot of activity on both virus and host sides. The long term goal of my lab is to understand this equilibrium and its consequences for the host.