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Blood, 15 December 2000, Vol. 96, No. 13, pp. 4055-4063
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Characterization of Epstein-Barr virus-infected B cells in
patients with posttransplantation lymphoproliferative disease:
disappearance after rituximab therapy does not predict
clinical response
Jie Yang,
Qian Tao,
Ian W. Flinn,
Paul G. Murray,
Linda E. Post,
Hong Ma,
Steven Piantadosi,
Michael A. Caligiuri, and
Richard F. Ambinder
From the Oncology Center, Johns Hopkins University
School of Medicine, Baltimore, MD; Department of Pathology, University
of Birmingham Medical School, United Kingdom; Comprehensive Cancer
Center, The Ohio State University, Columbus, OH.
Post-transplantation lymphoproliferative disease (PTLD) is
associated with Epstein-Barr virus (EBV). Quantitative and qualitative differences in EBV in peripheral blood mononuclear cells (PBMCs) of
PTLD patients and healthy controls were characterized. A quantitative competitive polymerase chain reaction (QC-PCR) technique confirmed previous reports that EBV load in PBMCs is increased in patients with
PTLD in comparison with healthy seropositive controls (18 539 vs 335 per 106 PBMCs, P = .0002). The average
frequency of EBV-infected cells was also increased (271 vs 9 per
106 PBMCs, P = .008). The distribution in
numbers of viral genome copies per cell was assessed by means of QC-PCR
at dilutions of PBMCs. There was no difference between PTLD patients
and healthy controls. Similarly, no differences in the patterns of
viral gene expression were detected between patients and controls.
Finally, the impact of therapy on viral load was analyzed. Patients
with a past history of PTLD who were disease-free (after chemotherapy or withdrawal of immunosuppression) at the time of testing showed viral
loads that overlapped with those of healthy seropositive controls.
Patients treated with rituximab showed an almost immediate and dramatic
decline in viral loads. This decline occurred even in patients whose
PTLD progressed during therapy. These results suggest that the
increased EBV load in PBMCs of PTLD patients can be accounted for by an
increase in the number of infected B cells in the blood. However, in
terms of viral copy number per cell and pattern of viral gene
expression, these B cells are similar to those found in healthy
controls. Disappearance of viral load with rituximab therapy confirms
the localization of viral genomes in PBMCs to B cells. However, the
lack of relationship between the change in viral load and clinical
response highlights the difference between EBV-infected PBMCs and
neoplastic cells in PTLD.
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