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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.
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