Associate Professor; School of Medicine / Department of Microbiology & Immunology
Area of interest
My lab studies the underlying mechanisms that stimulate immune responses to virus infections. We characterize the molecular and host-genetic pathways that lead to antiviral T cell responses, as well as pathogenic outcomes to infection. We work with lymphocytic choriomeningitis virus (LCMV) and HAV infections in mouse models and have several ongoing projects:
- We are examining the role of a histone demethylase in T cell-mediated immune defense against disseminated virus infection. We are currently characterizing specific genes and pathways that are regulated by UTX in T cells and are needed for immune control of infection.
- We are using forward genetics in mice to identify mutations responsible for a severe immunopathological response to systemic LCMV infection that is associated with elevated cytokines, thrombocytopenia, and lung edema, features resembling human arenavirus infection.
- Obesity is associated with worsened outcomes to virus infection in people. We identified a novel population of virus-specific T cells that is present in adipose tissue of infected mice. Obesity greatly increases the abundance of these cells, but results in an unusual form of pathogenesis upon re-infection, characterized by fat necrosis and pancreatitis. We are investigating how T cells are recruited to adipose, how obesity increases memory T cell numbers, and how T cells contribute to pathogenesis during infection.
- In close collaboration with Stan Lemon’s lab (UNC), we have developed the first mouse model of human hepatitis A virus infection. The infected mice replicate virus to high titers and develop lesions in the liver. We have identified several innate virus-sensing pathways that are critical for immune defense against this infection. We are dissecting how HAV disarms immune defenses in the liver and evaluating the molecular mechanisms associated with HAV-associated pathogenesis.