Epstein–Barr virus (EBV) is an extremely successful human herpesvirus which infects B cells of more than 90% of the adult population world-wide. Despite being ubiquitous, however, EBV rarely causes serious disease in the immunocompetent host due to a finely tuned balance between persistent infection and immune control mediated by virus-specific cytotoxic T lymphocytes (CTL). During immunosuppression, however, this balance is tipped in favour of the virus which encodes growth-transforming genes and is thus tumorigenic. In immunosuppressed organ transplant recipients, release from host immune control promotes uncontrolled proliferation of EBV-infected B cells which can ultimately culminate in outgrowth of EBV+ve post-transplant lymphoproliferative disease (PTLD). PTLD is aggressive, difficult to treat and fatal in up to 70% of cases despite current treatment and thus a major post-operative complication of transplant surgery. As PTLD biopsy material is very limited and PTLD-derived cell lines do not accurately reflect the lesions, the tumours have been modelled in animals in order to understand the pathogenesis of the disease as well as to test novel therapeutic regimes which are urgently needed.
|Journal||Reviews in Medical Virology|
|Publication status||Published - Jul 2002|