Immune surveillance of EBV-infected B cells and the development of non-Hodgkin lymphomas in immunocompromised patients.

After infection with the Epstein - Barr virus, a common gammaherpes virus which infects and persists in the B cells, an equilibrium is established in which newly infected and differentiating B cells are controlled by cytotoxic T cell (CTL) responses. Disturbance of this equilibrium, which can occur in immunocompromised situations, can lead to uncontrolled lymphoproliferation and subsequent development of non-Hodgkin Lymphomas (NHL). Here, we review the role of immunesurveillance of EBV-infected B cells and two situations where immunesurveillance is altered because of immunodeficiencies, transplantation recipients and HIV infection, which can lead to EBV-mediated NHL. In transplant recipients, immunosuppression prior and during transplantation can lead to lack of immunesurveillance and results in proliferation of infected B cells, which would normally be controlled by CTL responses. Interestingly, in HIV infection both deregulation of the normal B cell biology and a reduction in immunity play a role in developing NHL. Therefore, the nature of EBV infection in HIV-positive subjects is very different from that in transplanted individuals, in whom (re-)appearance of EBV-specific CD8(+) T cells - either by a decrease in immune suppression or infusion of donor lymphocytes - immediately leads to a decrease in EBV load.