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The biology of Epstein–Barr virus in post‐transplant lymphoproliferative disease
Author(s) -
Hsieh W.S.,
Lemas M.V.,
Ambinder R.F.
Publication year - 1999
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1034/j.1399-3062.1999.010308.x
Subject(s) - medicine , immunology , epstein–barr virus , lymphoproliferative disorders , lytic cycle , disease , immune system , virus , lymphoproliferative disease , cytotoxic t cell , transplantation , post transplant lymphoproliferative disorder , epstein–barr virus infection , virology , lymphoma , biology , pathology , in vitro , biochemistry
Post‐transplant lymphoproliferative disease (PTLD) is a B cell proliferative disorder that is associated with Epstein–Barr virus (EBV), an ubiquitous herpesvirus. EBV‐seronegative organ transplant recipients are at highest risk. EBV infection in PTLD lesions exists in a latent rather than lytic state, making tumor regression in response to antiviral agents unlikely. Viral latency proteins drive proliferation of T cells but also allow T cells to target PTLD lesions for destruction. Augmentation of the cellular immune response via the infusion of EBV‐specific cytotoxic T cells has yielded promising results in the prevention and treatment of PTLD in bone marrow transplant recipients. Efforts to extend this strategy to solid organ transplant recipients are ongoing. Editor’s comment: The spectrum of post‐transplant lymphoproliferative disease includes both B‐ and T‐cell malignancies. While the vast majority are EBV‐associated, there is a growing subset without obvious EBV markers. Given the present state of the art, which is summarized in this paper, we are incapable of stratifying patients in terms of prognosis or the likelihood of clinical response to reduction in immune suppression or to chemotherapy. The goal for multicenter trials must include the development of uniform definitions for the clinical and virologic manifestations of PTLD, as well as further attempts to define the natural history of this group of diseases. Jay A. Fishman, M.D.