Benjamin Gewurz

We study how Epstein-Barr virus causes nearly 1% of all human  cancers and also serves as the major viral trigger for autoimmune diseases, in particular multiple sclerosis.

A fascinating and incompletely understood aspect of EBV pathogenesis is that it causes different diseases in different populations and geographies.  EBV causes infectious mononucleosis and is associated with ~30% of Hodgkin lymphomas. With malaria or HIV co-infection, EBV is a major cause of Burkitt lymphoma. It causes tumors after transplantation, and interestingly also causes T cell and NK cell lymphomas. EBV also causes stomach cancers and nasopharyngeal carcinoma. With regards to autoimmunity, EBV infection appears to be a pre-condition for multiple sclerosis, and patients with MS have higher levels of antibodies against EBV proteins than people without MS.  EBV is now implicated in the pathogenesis of a growing number of autoimmune diseases. While much remains unknown about how EBV causes these diseases, they are very likely rooted in the viral lifecycle, which uses latency and lytic programs to navigate the B-cell compartment and colonize the memory cell reservoir.

We use CRISPR genetic, proteomic, metabolomic, biochemical and immunological approaches to study EBV pathogenesis and EBV/host interactions. We leverage a range of model systems, including tonsil organoid models of EBV infection or EBV co-infection with other pathogens, including HIV. We seek to mechanistically define how key EBV oncogenes and lytic cycle proteins work. We seek to define exactly how the viral lytic switch works, with an eye towards leveraging this knowledge in novel oncolytic therapeutic approaches. We also study how EBV remodels key oncometabolism and cell death pathways, including ferroptosis, and to identify how EBV evades and remodels innate and adaptive immune pathways to persistently infect 95% of adults worldwide and to trigger autoimmunity.

We are highly collaborative and enjoy working with many labs in the community.