Case studies : Epstein-Barr virus and cytomegalovirus infections

Epsein-Barr virus (EBV) is a member of the herpesvirus family. It is a DNA-encapsidated virus responsible for infectious mononucleosis, present in 90% of the adult population. Its particularity lies in its capacity to persist in a latent state, invisible to the immune system, within the body's host cells (B lymphocytes), and in its ability to cause lymphomas (around 200,000 cases worldwide each year). The EBV virus enters B lymphocytes by interaction of its envelope with a membrane receptor, CD21. Within the B lymphocytes, the viral genome can be replicated, resulting in the production of viral particles, the propagation of infection and cell death. It may also express a limited genetic program: my "type III latency", which causes B lymphocytes to proliferate and activate, without producing viral particles. The host's immune response, essentially linked to T lymphocytes, is directed at these two types of infection. The result is the destruction of infected cells, but also the persistence of B lymphocytes carrying the viral genome in episomal form, without the production of viral RNA and proteins. The kinetic and specificity components of T and B responses to EBV are now well understood. The study of EBV-induced immunopathological phenomena of a genetic nature has led to a better understanding of the phases of expansion and differentiation into cytotoxic T lymphocytes in the control of viral infection. Key molecules required for a T (and NK) immune response targeting B lymphocyte infection have been characterized. The mechanisms responsible for the genesis of cancers associated with chronic EBV infection (Hodgkin and non-Hodgkin lymphoma, T/NK lymphoma, gastric cancer, etc.) were discussed. Finally, the current issue of protection against EBV by vaccination was raised.