Download Epstein-Barr Virus and Human Cancer by B. Sugden, E. R. Leight (auth.), Professor Dr. Kenzo Takada PDF

By B. Sugden, E. R. Leight (auth.), Professor Dr. Kenzo Takada (eds.)

In this publication, notable researchers from the USA and Japan evaluation contemporary development in Epstein-Barr virus learn. most folks hold EBV in reminiscence B-cells in a latent degree. Many malignancies equivalent to T/NK telephone lymphoma, AIDS-associated B-cell lymphoma, gastric carcinoma and Hodgkin's disorder were causally associated with EBV. the improvement of molecular biology process has allowed us to review the jobs of person EBV genes that act within the upkeep and disruption of EBV latency.

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The DS element of oriP in the circular episomal DNA functions as a replication origin. As it replicates once in a single S phase, it is possible that oriP is regulated by the cellular replication licensing mechanism including the MCM family of replication licensing factors. Transient replication analysis using the oriP plasmid and HeLa/EBI cells revealed that the DS element requires early G 1 phase for the next round of replication, the same cell-cycle window in which the replication licensing of cellular chromatin occurs.

When BL cells are transferred in vitro and established as a cell line, this restricted pattern of EBV gene expression is not usually maintained and eventually replaced by latency III. Epstein-Barr Virus Nuclear Protein 2-lnduced Activation 41 The Burkitt's lymphoma line Akata, derived from a Japanese case of BL, is unique in that it maintains the latency I phenotype after long-term culture (TAKADA et al. 1991). Another unique property of Akata cells is that they have a tendency to lose EBV genomes spontaneously and to give rise to virus-negative sublines (SHIMIZU et al.

Nature 375:421--424 Marechal V, Dehee A, Chikhi-Brachet R, Piolot T, Coppey-Moisan M, Nicolas JC (1999) Mapping EBNA-I domains involved in binding to metaphase chromosomes. J Virol 73:4385--4392 Matsuo T, Heller M, Petti L, Oshiro E, Kieff E (1984) Persistence of the entire EBV genome integrated into human lymphocyte DNA. Science 226:1322-1325 Middleton T, Sugden B (1992) EBNAI can link the enhancer element to the initiator element of the Epstein-Barr virus plasmid origin of DNA replication. J Virol 66:489--495 Middleton T, Sugden B (1994) Retention of plasmid DNA in mammalian cells is enhanced by binding of the Epstein-Barr virus replication protein.

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