The focus of my research career has been to understand the mechanisms used by oncogenic gammaherpesviruses, to establish and maintain a life-long latent infection. Epstein-Barr virus (EBV) is a human specific oncogenic virus that establishes a life-long latent infection. Significantly, dysregulation of this long-term infection can lead to the development of malignancies, jeopardizing the life of the host. The predominate model of EBV latency, based on studies of EBV type 1 (EBV-1), posits that this virus has evolved to infect B cells and co-opt natural B cell activation pathways, such that infection of naïve B cells results in their activation and subsequent differentiation to memory B cells, where the virus latently resides. My work focuses on expanding this prevailing model. EBV is classified into two types EBV-1 and EBV-2, based on genetic variations. I have shown that the EBV types also differ in cell tropism. EBV-2, unlike EBV-1, has a unique tropism for T cells, infecting both B and T lymphocytes. The infection of T cells resulted in activation, proliferation, as well as alteration of cytokine expression demonstrating that EBV-2 has the ability to modulate normal T cell processes. EBV-2 infection of T cells has been observed in healthy children and in an EBV-2 mouse model, strongly suggesting that infection of T cells is a natural part of the EBV-2 life-cycle. Thus, shifting our view of EBV biology, uncovering the potential role of T cells in EBV-2 latency establishment, persistence, and lymphomagenesis. The broad research interest of the lab is to understand EBV-2 biology, specifically elucidating the significance of EBV-2 infection of T cells and the origins of EBV-2 associated lymphomas.
