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J. Virol., 02 1995, 871-881, Vol 69, No. 2
LD Klaman and DA Thorley-Lawson
Epstein-Barr virus (EBV) infection of mature, resting B cells drives them
to become lymphoblasts expressing high levels of cell surface molecules,
such as CD48, characteristically expressed on normal activated B cells.
Here, we report on the identification of an enhancer element in the CD48
gene which reproducibly confers strong transcriptional activity only in
EBV-positive B-lymphoblastoid cell lines. The element is not activated upon
infection of established EBV- negative B-cell lines, indicating that EBV
fails to drive these cells to a fully lymphoblastoid phenotype. An NF-kappa
B binding site is an essential component of the element but alone is not
sufficient to account for the activity or the specificity of the element.
We have detected a specific nuclear protein complex that binds to the
element and show that NF-kappa B1 (p50) is a part of this complex. The EBV-
encoded latent membrane protein 1 is capable of transactivating the
isolated CD48 NF-kappa B site but not the intact element, suggesting that
the latent membrane protein 1-driven activation of NF-kappa B/Rel must
interact with other regulatory pathways to control expression of cellular
genes as EBV drives resting B cells into the cell cycle.
Copyright © 1995, American Society for Microbiology
Characterization of the CD48 gene demonstrates a positive element that is specific to Epstein-Barr virus-immortalized B-cell lines and contains an essential NF-kappa B site
Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111.
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