The overall aim of the Viral Pathogenesis Lab is to gain an understanding of the basic molecular mechanisms involved in the modulation of cellular function by herpesviruses. Herpesviruses are a major cause of disease worldwide and are amongst the most successful human pathogens, with specific viruses infecting more than 90% of the world's population. The main biological feature of these viruses is their ability to persist and reactivate in a primed immunocompetent host.
The control of herpesviruses infections thus represents an important clinical goal. To achieve this we must first understand the basic mechanisms of viral pathogenesis. We use a laboratory animal model of infection with murine gamma-herpesvirus-68 (MHV-68), which establishes latent infection in B-lymphocytes. The ability to genetically manipulate both the virus and the host allows the dissection of the molecular mechanisms involved in the virus/host interaction.
We have recently identified viral proteins that are essential for the effective establishment of latent infection. One of these, M2, functions as an adaptor protein that assembles a signalosome with cellular proteins involved in the activation and differentiation of B lymphocytes, and which we have shown to be essential for the establishment of latent infection.