Jason Kyle Whitmire

PhD
Associate Professor; School of Medicine / Department of Microbiology & Immunology
UNC-Chapel Hill
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:

  1. 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.
  2. 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.
  3. 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.
  4. 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.