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Epstein-Barr viral DNA in acute large granular lymphocyte (natural killer)
leukemic cells [see comments]
DN Hart, BW Baker, MJ Inglis, JC Nimmo, GC Starling, E Deacon, M Rowe and ME Beard
Haematology Department, Christchurch Hospital, New Zealand.
Serologic studies in a male Caucasian presenting with an acute
hepatitis-like illness, associated with an increase in peripheral blood
large granular lymphocytes (LGLs), suggested a chronic or reactived
Epstein-Barr virus (EBV) infection. The LGL were shown to have a natural
killer (NK) cell, CD3- CD16- CD56+ CD57- phenotype and mediated strong
nonspecific major histocompatability complex-unrestricted (NK) cytotoxic
activity. A progressive increase in the peripheral blood LGL count was
associated with a rapid deterioration, hepatic necrosis, and death.
Widespread organ infiltration with LGLs suggested a malignant
lymphoproliferative condition, but no lymphoid (T-cell receptor or IgH)
gene rearrangement or cytogenetic marker was detected. However, molecular
analysis identified EBV genomic DNA present in a single episomal form
within the LGL, establishing the clonal nature of the LGL proliferation.
Confirmation that the EBV had infected the leukemic LGL was obtained by in
situ hybridization studies that showed EBV RNA within the LGLs.
Immunoblotting of LGL protein extracts established that, of the EBV gene
products, EBV nuclear antigen-1 (EBNA-1) was expressed but EBNA-2 and the
latent membrane protein (LMP-1) were not detectable in the leukemic cells.
These results suggest that EBV may be involved directly in LGL cell
transformation, in a manner similar to EBV-associated B-cell lymphomas,
although other molecular changes probably contribute to the evolution of a
fully malignant leukemic clone.
Volume 79,
Issue 8,
pp. 2116-2123,
04/15/1992
Copyright © 1992 by The American Society of Hematology
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