• Ph.D., Northwestern University, 1980

Research Interests: The research in my lab focuses on 2 gamma-herpesviruses, Epstein-Barr virus (EBV) and murine gamma herpesvirus 68 (gHV68). A major property of all herpesviruses is their ability to persist for life in the infected individual. The gamma-herpesviruses are known to latently infect either B or T lymphocytes, and to be associated with the development of lymphoma and lymphoproliferative diseases. Our major interests are to understand: (i) how these viruses regulate viral gene expression during latency; (ii) how they modulate and avoid the host immune response; and (iii) how they switch from a latent infection to replication of the viral genome (referred to as reactivation), a process that is essential for propagation of these viruses to uninfected individuals. EBV is the etiologic agent of infectious mononucleosis and is closely associated with the development of Burkitt's lymphoma, nasopharyngeal carcinoma, 30-50% of Hodgkin's disease, and 50% of lymphomas that arise in immunosuppressed individuals (e.g., transplant patients and AIDS patients). Our research on EBV focuses on tissue culture models that recapitulate the various EBV genetic programs. The information gained from these studies is then employed to address the behavior of EBV in infected individuals. However, because there are no small animal models for studying EBV pathogenesis, we use gHV68 infection of mice to address specific issues of the host response to gamma-herpesvirus infection. The advantage of the latter model is that both the host and pathogen can be genetically manipulated to address fundamental aspects of host-pathogen interactions. gHV68 infection of mice causes several different chronic diseases in immunocompromised mice, including a severe vasculitis that affects the great elastic arteries and lymphoproliferative disease. We are currently identifying gHV68 genes involved in establishing and maintaining viral latency, as well as those involved in the development of chronic disease. In addition, we are actively characterizing the host response to viral infection to address how viral latency and persistent infection is controlled.