Introduction

More than 90% of the adult human population is infected by Epstein-Barr virus (EBV). Infection takes place early in life and then persists life-long. EBV is the causative agent for infectious mononucleosis (glandular fever), but most EBV carriers show no symptoms or pathology at the time of infection. However, EBV is strongly associated with a number of human tumors such as nasopharyngeal carcinoma, gastric cancer, Burkitt’s lymphoma, immunosuppression-related lymphomas, Hodgkin’s disease, and others. 11% of viral associated human cancers are associated with EBV.

EBV infects human B lymphocytes and certain epithelial cells in vitro and in vivo. After infection of resting B-lymphocytes, the virus reactivates the cells and induces their indefinite proliferation (immortalization) by establishing a latent infection (i.e. the cells do not release virus). The infected cells carry several copies of the EBV episome and express a subset of the viral genes (the so-called latent genes). These viral latent genes contribute to the induction and maintenance of B-cell proliferation. It is now well accepted that replication of EBV is an important step before the appearance of the pathologies.

In our lab, we are studying the mechanisms by which EBV induces B cells immortalization and the regulation of the switch between latent persistence and virus replication. We focus our study on the biological role of some key viral genes that contribute to these processes at the genetic, molecular and cellular levels.