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Replication Licensing of the EBV oriP Minichromosome

  • Chapter
Epstein-Barr Virus and Human Cancer

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 258))

Abstract

In human B lymphocytes latently infected in vitro and in vivo with Epstein-Barr virus (EBV), including Burkitt’s lymphoma (BL) cells and various other EBV-related tumor cells, the viral DNA persists mostly in a circular episomal form with multiple copies and expresses a limited number of viral genes, while some of the latent EBV DNA may be integrated into the host chromosomal DNA (Kieff 1996; Hirai et al. 1998 for review). The original definition of the term “episome” coined by Jacob and Wollman (1961) is a genetic factor that can persist in both the integrated state and as an extrachromosomal replicon in host cells. However, the term episome has also been used to describe the circular, extrachromosomal plasmid state of the latent EBV genome in most recent papers related to the state of latent EBV. We also follow this definition.

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  1. Department of Tumor Virology, Division of Virology and Immunology,Medical Research Institute, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo, Tokyo, 113-8510, Japan

    K. Hirai & M. Shirakata

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  1. K. Hirai
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  2. M. Shirakata
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  1. Institute for Genetic Medicine, Department of Tumor Virology, Hokkaido University, N15 W7, Kita-Ku, 060-8638, Sapporo, Japan

    Kenzo Takada

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Hirai, K., Shirakata, M. (2001). Replication Licensing of the EBV oriP Minichromosome. In: Takada, K. (eds) Epstein-Barr Virus and Human Cancer. Current Topics in Microbiology and Immunology, vol 258. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56515-1_2

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