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Failure to detect Epstein-Barr virus DNA in peripheral blood mononuclear
cells of most patients with large granular lymphocyte leukemia
TP Loughran , R Zambello, R Ashley, J Guderian, M Pellenz, G Semenzato and G Starkebaum
Fred Hutchinson Cancer Research Center, University of Washington School of
Medicine, Seattle.
Clonal disease of large granular lymphocytes (LGLs) may arise from either
CD3+ LGLs (LGL leukemia) or CD3- LGLs (natural killer [NK] cell leukemia).
Other patients have chronic LGL proliferations that cannot be proven to be
clonal (lymphoproliferative disease of granular lymphocytes [LDGL]). It was
recently shown that clonally expanded CD3- LGLs from Japanese patients
contain Epstein-Barr virus (EBV) DNA sequences, arguing for a direct
causative role for EBV in NK cell leukemia. The aggressive clinical course
and other clinical features of these Japanese patients differ markedly from
the clinical features of LGL leukemia and CD3- LDGL patients in the United
States and Europe, suggesting different pathogenic mechanisms. Therefore,
we performed serologic and DNA hybridization studies for EBV in 31 patients
from the United States and Europe (18 with LGL leukemia and 13 with chronic
CD3- LDGL). All patients had serologic evidence for past infection with
EBV. We did not detect EBV DNA sequences in peripheral blood mononuclear
cell DNA from any of these patients in Southern blot hybridization
analyses. EBV DNA sequences were detected after polymerase chain reaction
amplification of peripheral blood mononuclear cell DNA in only 2 of 18 LGL
leukemia patients and 4 of 13 chronic CD3- LDGL patients. These results
argue against a direct causative role for EBV infection in LGL leukemia or
chronic CD3- LDGL occurring in the United States and Europe.
Volume 81,
Issue 10,
pp. 2723-2727,
05/15/1993
Copyright © 1993 by The American Society of Hematology
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