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Journal of Virology, September 2009, p. 9163-9174, Vol. 83, No. 18
0022-538X/09/$08.00+0     doi:10.1128/JVI.01979-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Distinctive Effects of the Epstein-Barr Virus Family of Repeats on Viral Latent Gene Promoter Activity and B-Lymphocyte Transformation{triangledown}

Ahmed K. M. Ali,1,2 Satoru Saito,1,2 Sachiko Shibata,2 Kenzo Takada,1 and Teru Kanda2*

Department of Tumor Virology,1 Research Center for Infection-Associated Cancer, Institute for Genetic Medicine, Hokkaido University, N15 W7, Kita-ku, Sapporo 060-0815, Japan2

Received 19 September 2008/ Accepted 22 June 2009

The Epstein-Barr virus (EBV), a human B-lymphotropic gamma herpesvirus, contains multiple repetitive sequences within its genome. A group of repetitive sequences, known as the family of repeats (FR), contains multiple binding sites for the viral trans-acting protein EBNA-1. The FR sequences are important for viral genome maintenance and for the regulation of the promoter involved in viral latent gene expression. It has been reported that a palindromic sequence with a putative secondary structure exists at the 3' end of the FR in the genome of the EBV B95-8 strain and that this palindromic sequence has been deleted from the FR of the commonly used EBV miniplasmids. For the first time, we cloned an EBV B95-8 DNA fragment containing the full-length FR, which enabled us to examine the functional difference between full-length and deleted FRs. The full-length FR, like the deleted FR, functioned as a transcriptional enhancer of the viral latent gene promoter, but that transactivation was significantly attenuated in the case of the full-length FR. No significant enhancement of replication was observed when the deleted FR was replaced with the full-length FR in an EBV miniplasmid. By contrast, when the same set of FR sequences were tested in the context of the complete EBV genome, the full-length FR resulted in more-efficient B-cell transformation than the deleted FR. We propose that the presence of the full-length FR contributes to the precise regulation of the viral latent promoter and increases the efficiency of B-cell transformation.

* Corresponding author. Present address: Division of Virology, Aichi Cancer Center Research Institute, 1-1, Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. Phone: 81-52-762-6111. Fax: 81-52-763-5233. E-mail: tkanda{at}aichi-cc.jp

{triangledown} Published ahead of print on 1 July 2009.

Journal of Virology, September 2009, p. 9163-9174, Vol. 83, No. 18
0022-538X/09/$08.00+0     doi:10.1128/JVI.01979-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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