EBV Gene Expression, EBNA Antibody Responses and EBV⁺Peripheral Blood Lymphocytes in Post-Transplant Lymphoproliferative Disease

Abstract

Epstein-Barr virus (EBV) is associated with the development of several B cell malignancies including Burkitt's lymphoma (BL), post-transplant lymphoproliferative disease (PTLD), and AIDS-related lymphomas. The latter two diseases result from EBV-driven B cell proliferation in the absence of normal immunosurveillance and as such, represent a heterogenous family of lymphoproliferative disorders. This article reviews studies on EBV gene expression and antibody development in PTLD and introduces recent information on the levels of EBV+ peripheral blood lymphocytes to discuss possible mechanisms of pathogenesis under varying conditions of immunosuppression.

Microbiome and Malignancy

“…EBV latency becomes disrupted in PTLD, diseases related to the intersection of 20 th Century medical technologies with an ancient virome constituent. PTLD lesions express EBV Latency III genes, the encoded proteins involved in signal transduction, transcription, protein catabolism, and cell motility, shape, and adhesion characteristics (Carter et al, 2002; Delecluse et al, 1995; McKnight et al, 1994; Rea et al, 1994). Impaired α-EBV T-cell function permits EBV-driven B-cell proliferation resulting in PTLD.…”

Posttransplant lymphoproliferative disease in a child: clinical and molecular characterization

“…Under normal immune surveillance the infection is self-limited, because B cells, which express EBV-antigens, are eliminated by the immune system. Under immunosuppressive therapy a reactivation of latent EBV or a primary EBV infection takes place, and a spectrum of EBV-driven B cell proliferations can develop [34]. As a hypothesis, EBV infection leads to polyclonal B cell proliferation.…”

Pathology of Pediatric Gastrointestinal and Liver Disease

“…Of these, 49 % were seronegative and 75 % of these acquired primary infection. This requires prompt reduction of immune suppression and use of antiviral drugs (Lee et al 2005 ;McKnight et al 1994 ;Renard et al 1991 ). The presence of IgM anti-VCA titer, the absence of anti-Epstein-Barr nuclear antigen (EBNA), and the presence of a heteroagglutination titer are diagnostic of primary infection.…”