PhD Student in the Department of Molecular Genetics & Microbiology
Synopsis: Herpesviruses support two modes of infection: Lytic replication and latency. Gammaherpesviruses (γHV) establish latency in B lymphocytes and their latent programs are associated with the development of lymphomas. Investigating the role of both virus and host determinants in promoting the establishment and reactivation from latency is an important area of investigation for the γHV. The human γHV, Epstein-Barr Virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), co-opt host NF-κB signaling pathways to promote latency establishment, virus gene regulation and cell survival. Disruption of the NF-κB signaling pathway poses a potential therapeutic target as it induces the apoptosis of EBV+ and KSHV+ lymphomas in culture and delays tumor progression of these cells in mice. Our laboratory made similar observations for murine γHV 68 (MHV68) latently infected B cells.The purpose of my project is to define the importance of this virus-host interaction in promoting B cell latency during γHV infection.