Abstract
Epstein-Barr virus (EBV), a prevalent human herpesvirus, is maintained as an extrachromosomal, multicopy plasmid in latently infected B cells. Latent infection is characterized by limited viral gene expression (Epstein and Achong 1979; van Santon et al. 1981) and faithful replication of the EBV episome once (and only once) per cell cycle in parallel with cellular DNA (Adams 1987; Hamper et al. 1974). The EBV replicon, in contrast to the “runaway” replication characteristic of polyomaviruses, provides a model for the study of a replication origin regulated by and within the cell cycle. EBV plasmid replication is particularly attractive for this because only two viral genetic elements are required for plasmid maintenance: a cis-acting replication origin within the EBV BamHI C region (Lupton and Levine 1985; Reisman et al. 1985; Yates et al. 1984) and the transacting EBV nuclear antigen 1 (EBNA-1) (Lupton and Levine 1985; Reisman et al. 1985). It seems likely, therefore, that EBV plasmid maintenance will be closely regulated by cellular mechanisms that initiate replication of host cell chromosomes and permit only one duplication cycle per generation.
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© 1989 Springer-Verlag Berlin · Heidelberg
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Frey, A., Chittenden, T., Levine, A.J. (1989). Epstein-Barr Virus DNA Replication. In: Knippers, R., Levine, A.J. (eds) Transforming Proteins of DNA Tumor Viruses. Current Topics in Microbiology and Immunology, vol 144. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74578-2_28
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DOI: https://doi.org/10.1007/978-3-642-74578-2_28
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