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Blood, Vol. 94 No. 1 (July 1), 1999:
pp. 244-250
EBNA-1 Gene Sequences in Brazilian and American Patients With
Hodgkin's Disease
Karen L. Chang,
Yuan-Yuan Chen,
Wen-Gang Chen,
Kazuhiko Hayashi,
Carlos Bacchi,
Maura Bacchi, and
Lawrence M. Weiss
From Division of Pathology, City of Hope National Medical Center,
Duarte, CA; Department of Pathology, Okayama University Medical School,
Okayama, Japan; and Department of Pathology, State University of Sao
Paulo (UNESP), Botucatu, Brazil.
We examined the types of Epstein-Barr virus-associated nuclear
antigen-1 (EBNA-1) gene carboxy (C)-terminal mutations
occurring in Hodgkin's disease (HD) and reactive tissues from two
different geographic regions. Previously reported EBNA-1 C-terminal
region amino acid sequence variants, based on the amino acid at codon 487, include Prototype (P)-ala, which is found in the B95.8-derived prototype virus, P-thr, Variant (V)-leu, V-val, and V-pro. Using polymerase chain reaction (PCR) to amplify portions of the
EBNA-1 gene, followed by DNA sequencing, we found a single EBNA-1 gene sequence variant in each tissue, whether reactive or neoplastic and
whether from Brazil or the United States. Variant EBNA-1 gene sequences
were more common in both neoplastic and non-neoplastic tissues from
different geographic areas than the so-called prototype sequence. In
the 17 Brazilian HD cases, 4 cases had P-thr variants and 13 had V-leu
variants. In the six reactive tissues from Brazil, one had a P-ala
variant, two had P-thr variants, and three had V-leu variants. In the
12 American HD cases, 2 had P-ala variants, 6 had P-thr variants, and 4 had V-leu variants. The 11 American reactive tissues included 2 P-ala
variants, 5 P-thr variants, and 4 V-leu variants. In both countries,
there were similar variant EBNA-1 sequences present in normal tissues
and HD cases. Compared with the P-ala and P-thr cases, the V-leu cases
were more likely to have the 30-bp latent membrane protein 1 (LMP1) gene deletion (P = 0.0075). In
addition, cases of HD with the V-leu were statistically associated with
a substitution of asparagine for glutamine at codon 322 of the
C-terminal portion of the LMP1 gene. Our results suggest that any
variation in EBNA-1 gene sequence is caused by a polymorphism present
in pre-existing viral strains in the underlying population, and not a
mutation occurring during oncogenesis.
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