Abstract
Infection of human B lymphocytes with the Epstein-Barr virus (EBV) can lead to the establishment of a latent infection with concomitant immortalization of these cells (1–3). Within the immortalized cell the viral genome exists predominantly as a circular plasmid (4–7) and exhibits limited transcriptional activity. At least six viral genes are expressed in the immortalized cell (8–11) and are presumed to be required for the maintenance of latency and in potentiating the growth of the cell (12). The EBV nuclear antigen-1 (EBNA-1), encoded by the BamHI-K fragment, belongs to this set of latency-related viral genes and has been found to be multifunctional within the immortalized cell. EBNA-1 appears to be the only viral gene product required for replication of plasmids possessing the EBV oriP (13, 14) and is therefore thought to be required for the maintenance of episomal EBV within the immortalized cell. EBNA-1 has also been implicated in regulation of its own transcription, as well as the transcription regulation of the EBNA family of genes (15, 16). This involvement of EBNA-1 with gene regulation was demonstrated when experiments revealed that the 30-bp repeat region of oriP functions as a transcriptional enhancer element that is trans-activated by EBNA-1.
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Nonoyama, M., Wen, LT., Tanaka, A., Bradley, G. (1990). Detection of 12-o-Tetradecanoylphorbol-13-Acetate-induced Cellular Proteins That Compete with the Epstein-Barr Virus Nuclear Antigen 1 (EBNA-1) for Binding to a Site within the Epstein-Barr Virus oriP . In: Lopez, C., Mori, R., Roizman, B., Whitley, R.J. (eds) Immunobiology and Prophylaxis of Human Herpesvirus Infections. Advances in Experimental Medicine and Biology, vol 278. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5853-4_13
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