Having survived millions of years of evolution amongst primates, Epstein Barr virus (EBV) is considered one of the most complicated viruses. It not only causes primary infectious mononucleosis but also has the ability to transform itself into an oncogenic virus to cause cancers like Nasopharyngeal carcinoma and Hodgkin's carcinoma. Recent evidence also strongly correlates EBV to various autoimmune diseases such as multiple sclerosis and systemic lupus erythematosus.
These diseases are usually treated with traditional approaches including ectomy and radio/chemotherapy, with the addition of monoclonal antibodies in some cases. Limited therapeutic progress has led to increased interest in the capacity for immunotherapy in the targeted treatment of EBV associated diseases. Strong evidence supporting the role of dysfunctional T cells in EBV cancers, has already led to the development of immunotherapies for EBV lymphomas. However, this approach warrants further studies with regard to testing the efficacy, safety and prolonged survival of infused immune cells for the targeted attack of virus/ virus transformed cells in vivo.
As a part of my PhD project in the Translational and Human Immunology lab, at QIMRB, we have developed and characterized a humanized murine model that enables us to replicate latent EBV cancer in vivo. Using this model, my project aims to profile the immune landscape and evaluate immunotherapies in vivo.
Additionally, this model provides us with a platform to investigate the underlying immunological, virological and serological parameters of EBV associated lymphomas and other EBV-associated autoimmune conditions. It provides a powerful resource for the characterization of viral trafficking, and furthermore histopathology analysis enables us to demonstrate the spatial configuration of immune cells in relation to EBV virus and its various strains. Importantly, this model allows us to examine the temporal activity of cytotoxic lymphocytes as a therapy for EBV-associated tumors in varying EBV strain landscape.