Book Chapter10.1016/S0065-230X(08)61003-9
Epstein-Barr virus-associated lymphoproliferative disorders in immunocompromised individuals.
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TL;DR: Progress has been made in elucidating the structure and function of the EBV genome, thereby providing important insights into the oncogenic role of EBV in human neoplasia, and increasing awareness that EBV may be causally linked to a wide range of lymphoproliferative disorders.
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Abstract: Publisher Summary The Epstein–Barr virus (EBV) acts as one of a number of factors including environmental and genetic elements that contribute to the pathogenesis of Burkitt's lymphoma (BL) Apart from BL, EBV is associated with a wide spectrum of lymphoproliferative diseases that develop in a setting of inherited or acquired immunodeficiency A common factor in the development of these lesions is thought to be an underlying deficit in the normal immunoregulatory mechanisms that control EBV infection in vivo Through major advances in the field of molecular biology, progress has been made in elucidating the structure and function of the EBV genome, thereby providing important insights into the oncogenic role of EBV in human neoplasia There is also increasing awareness that EBV may be causally linked to a wide range of lymphoproliferative disorders in which impairment of EBV-specific host immunity appears to be an important underlying factor In many instances, EBV-related lymphoproliferative disorders in immune-compromised individuals fulfill established criteria for malignancy based on histology, evidence of clonality, and rapidly aggressive clinical course However, a proportion of these tumors developing in the context of iatrogenic immune suppression for organ and bone marrow transplantations undergoes complete resolution following the withdrawal of immunosuppressive therapy, either alone or in combination with antiviral agents The consensus is that the clinical, morphological, cytogenetic, and clonal heterogeneities of these tumors reflect a spectrum of changes through which a polymorphic, polyclonal hyperplastic process induced by EBV evolves to an oligoclonal and ultimately multiclonal or monoclonal malignant tumor population
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AIDS-associated non-Hodgkin lymphoma.
TL;DR: Investigation of the epidemiology and aetiology of AIDS-related non-Hodgkin lymphoma by analysing data from cases reported to the Centers for Disease Control, Atlanta, USA, up to June 30, 1989 suggested there was probably no single cause for all the types of lymphoma.
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Epstein-Barr virus and Hodgkin's disease: transcriptional analysis of virus latency in the malignant cells.
E M Deacon,G Pallesen,Gerald Niedobitek,John Crocker,L Brooks,Alan B. Rickinson,Lawrence S. Young +6 more
TL;DR: Preliminary results on viral gene expression in HRS cells are extended by adopting polymerase chain reaction-based and in situ hybridization assays capable of detecting specific EBV latent transcripts diagnostic of the different possible forms of EBV latency.
Activation and adoptive transfer of Epstein–Barr virus-specific cytotoxic T cells in solid organ transplant patients with posttransplant lymphoproliferative disease
Rajiv Khanna,Scott C. Bell,Martina Sherritt,Andrew J. Galbraith,Scott R. Burrows,Lee Rafter,B. E. Clarke,Richard Slaughter,Michael C. Falk,Jo A Douglass,Trevor Williams,Suzanne L. Elliott,Denis J. Moss +12 more
TL;DR: It is demonstrated that a potent EBV-specific memory response can be expanded from solid organ recipients who have acquired their primary EBV infection under high levels of immunosuppressive therapy and that these T cells may have therapeutic potential against PTLD.
356
Biology and disease associations of Epstein–Barr virus
TL;DR: Recent views on the EBV life cycle and its interlinks with normal B-cell biology are described, and how this interrelationship may be upset and result in EBV-associated disease is discussed.
294
Role of Cytotoxic T Lymphocytes in Epstein-Barr Virus-Associated Diseases
Rajiv Khanna,Scott R. Burrows +1 more
TL;DR: In this article, an overview of virus and the host immune system interactions that regulate the life-long host-virus relationship in healthy virus carriers and EBV-associated diseases is presented.
221
References
•Journal Article
Immune deficiency in the X-linked lymphoproliferative syndrome. I. Epstein-Barr virus-specific defects.
Shinji Harada,Kiyoshi Sakamoto,Janet K. Seeley,T Lindsten,Thomas Bechtold,J Yetz,G Rogers,Gary R. Pearson,David T. Purtilo +8 more
TL;DR: Most patients with XLP failed to effect regression of autologous EBV-infected lymphoblastoid cell lines, indicating a deficiency in long-lived T cell-mediated immunity to EBV.
79
Cytogenetic features of Hodgkin's disease suggest possible origin from a lymphocyte.
Fernando Cabanillas,Sen Pathak,Jennifer M. Trujillo,Grace Grant,Ann Cork,Fredrick B. Hagemeister,William S. Velasquez,P. McLaughlin,J. R. Redman,Ruth L. Katz +9 more
TL;DR: Tumor samples from 49 patients were studied to determine if any chromosomal abnormalities that could add further information to this controversial point are present, and the most common breakpoints were in 11q23, 14q32, 6q11-21, and 8q22-24.
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Epstein-barr virus infections in the x-linked recessive lymphoproliferative syndrome
DavidT. Purtilo,Jag Bhawan,LindseyM. Hutt,Lucian K. Denicola,I.O. Szymanski,JamesP.S. Yang,William Boto,Rorert Maier,David A. Thorley-Lawson +8 more
TL;DR: Variable phenotypic expression of the X-linked recessive lymphoproliferative syndrome probably resulted from the varied immune response to E.B.V, which can induce fatal I.R.M. and malignant lymphoma in X.L.S., but an immune responseto E.V. can be protective.
76
Epstein-Barr virus gene expression in malignant lymphomas induced by experimental virus infection of cottontop tamarins.
TL;DR: Since both proteins are known to be important effector molecules of virus-induced B-cell growth transformation in vitro, their expression in these lymphomas constitutes the best evidence for a direct oncogenic role for EBV in vivo.
72
Lymphadenopathy morphologically consistent with Hodgkin's disease associated with Epstein-Barr virus infection.
TL;DR: This case report describes a case of chronic Epstein-Barr virus infection resulting in lymphadenopathy morphologically indistinguishable from Hodgkin's disease, and for the first time in the literature, EBNA could be demonstrated in the nuclei of Sternberg-Reed cells.
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