Studying Epstein-Barr virus pathologies and immune surveillance by reconstructing EBV infection in mice

Abstract

Epstein-Barr virus (EBV) is a γ herpes virus endemic in humans and transforming human B lymphocytes. It causes a variety of human pathologies ranging from infectious mononucleosis upon acute infection to EBV-driven B-cell lymphomas. In humans, EBV-infected cells are under powerful immune surveillance by T and NK cells. If this immune surveillance is compromised as in immunosuppressed (AIDS- or posttransplantation) patients, the virus can spread from rare, EBV-containing cells and cause life-threatening pathologies. We have found that EBV immune surveillance and lymphomagenesis can be modeled in mice by targeted expression of key EBV proteins in the B-cell lineage. As EBV does not infect mouse B cells and mice have thus not coevolved with the virus, EBV exploits basic modes of the host immune response to optimize its coexistence with the host.