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Epstein-Barr Virus (EBV) in Endemic Burkitt's Lymphoma:
Molecular Analysis of Primary Tumor Tissue
Qian Tao,
Keith D. Robertson,
Angela Manns,
Allan Hildesheim, and
Richard F. Ambinder
From the Oncology Center, Johns Hopkins Medical Institutions,
Baltimore, MD, and the National Institutes of Health, Rockville, MD.
Many aspects of Epstein-Barr virus (EBV) and tumor biology have been
studied in Burkitt's lymphoma (BL)-derived cell lines. However, in
tissue culture, patterns of gene expression and CpG
methylation often change and viral strain selection may occur. In this
report, 10 cases of snap-frozen endemic BL tumors are characterized in
terms of viral gene expression, promoter usage, methylation, and viral
strain. EBNA1 and BamHI-A rightward transcripts (BART) were
detected in 7 of 7 and LMP2A transcripts in 5 of 7 tumors with
well-preserved RNA. Transcripts for the other EBNAs and for LMP1 were
not detected in any tumor. These tumors differ from BL cell lines in
that they lack a variety of lytic cycle transcripts. This pattern of
viral gene expression in endemic BL is similar to that reported in
peripheral blood mononuclear cells (PBMCs) from healthy
EBV-seropositive individuals. EBNA1 transcripts originated from the Q
promoter (Qp) but not C, W, or F promoters that drive transcription of
EBNA1 in other circumstances. Whereas Cp has been previously shown to
be entirely CpG methylated in BL, bisulfite genomic sequencing showed
virtually no methylation in Qp. Type-A EBV was detected in 6 of 10 and
type B in 4 of 10 cases. A previously reported 30bp deletion variant in
the carboxyl terminal of LMP1 gene was detected in 5 of 10 cases. The
association with both A and B strains contrasts with EBV-associated
Hodgkin's disease, nasopharyngeal carcinoma, and post-transplant
lymphoproliferative disease, which are much more consistently
associated with A strain virus.
Blood, Vol. 91 No. 4 (February 15), 1998:
pp. 1373-1381
© 1998 by The American Society of Hematology.
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