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Related Collections Immunobiology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2001, Vol. 98, No. 1, pp. 146-155 IMMUNOBIOLOGY Dysfunctional Epstein-Barr virus (EBV)-specific CD8+ T lymphocytes and increased EBV load in HIV-1 infected individuals progressing to AIDS-related non-Hodgkin lymphoma Debbie van Baarle, Egbert Hovenkamp, Margareth F. C. Callan, Katja C. Wolthers, Stefan Kostense, Linda C. Tan, Hubert G. M. Niesters, Albert D. M. E. Osterhaus, Andrew J. McMichael, Marinus H. J. van Oers, and Frank Miedema From the Department of Hematology; Department of Clinical Viro-Immunology, CLB, and Laboratory for Experimental and Clinical Immunology; and Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Molecular Immunology Group, Institute of Molecular Medicine, Oxford, United Kingdom; and Department of Virology, University Hospital Rotterdam, Rotterdam, The Netherlands. Acquired immunodeficiency syndrome-related non-Hodgkin lymphomas (AIDS-NHL) are thought to arise because of loss of Epstein-Barr Virus (EBV)-specific cellular immunity. Here, an investigation was done to determine whether cellular immunity to EBV is lost because of physical loss or dysfunction of EBV-specific cytotoxic T cells. Data on EBV-specific cellular immunity were correlated with EBV load. For comparison, individuals who progressed to AIDS with opportunistic infections (AIDS-OI) and long-term asymptomatics (LTAs) were studied. The number of virus-specific T cells was detected using tetrameric HLA-EBV-peptide complexes; function of these EBV-specific T cells was determined using the interferon- (IFN-) Elispot assay. It was observed that EBV-specific CD8+ T cells were present in normal numbers in human immunodeficiency virus (HIV)-infected individuals. However, their functional capacity was decreased compared with HIV individuals. In AIDS-NHL patients, EBV-specific T cells were not physically lost in the course of HIV-1 infection but showed progressive loss of their capability to produce IFN- in response to EBV peptides. This loss of function correlated with lower CD4+ T-cell numbers and was accompanied by increasing EBV load. In HIV-1-infected LTA individuals, in whom CD4+ T-cell numbers were maintained, and progressors to AIDS-OI, IFN--producing EBV-specific T cells were stable and EBV load remained stable or decreased in the course of HIV infection, suggestive of immune control. Our data indicate that functional loss of EBV-specific CD8+ T cells with a concomitant increase in EBV load may play a role in the pathogenesis of AIDS-NHL. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Plesa, A. E. Snook, S. A. Waldman, and L. C. Eisenlohr Derivation and Fluidity of Acutely Induced Dysfunctional CD8+ T Cells J. Immunol., April 15, 2008; 180(8): 5300 - 5308. [Abstract] [Full Text] [PDF] E. J. Wiertz, R. Devlin, H. L. Collins, and M. E. Ressing Herpesvirus Interference with Major Histocompatibility Complex Class II-Restricted T-Cell Activation J. 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	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020