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Journal of Virology, October 2007, p. 11236-11245, Vol. 81, No. 20
0022-538X/07/$08.00+0     doi:10.1128/JVI.00579-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus (EBV)-Encoded RNA 2 (EBER2) but Not EBER1 Plays a Critical Role in EBV-Induced B-Cell Growth Transformation{triangledown}

Yi Wu,1 Seiji Maruo,1 Misako Yajima,1 Teru Kanda,2 and Kenzo Takada1*

Department of Tumor Virology,1 Center for Virus Vector Development, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan2

Received 19 March 2007/ Accepted 27 July 2007

Epstein-Barr virus (EBV)-encoded RNA 1 (EBER1) and EBER2 are untranslated RNAs and the most abundant viral transcripts in latently EBV-infected cells. We previously reported that EBERs play a critical role in efficient EBV-induced growth transformation of primary B cells. To investigate whether EBER1 and EBER2 have distinct roles in B-cell growth transformation, recombinant EBVs carrying either EBER1 or EBER2 were generated. The transforming ability of recombinant EBVs expressing EBER2 was as high as that of EBVs expressing both EBER1 and EBER2. In contrast, the transforming ability of recombinant EBVs carrying EBER1 was impaired and was similar to that of EBV lacking both EBER1 and EBER2. Lymphoblastoid cell lines (LCLs) established with EBVs carrying EBER2 proliferated at low cell densities, while LCLs established with EBVs carrying EBER1 did not. Interleukin 6 (IL-6) production in LCLs expressing EBER2 was more abundant than in those lacking EBER2. The growth of LCLs lacking EBER2 was enhanced by the addition of recombinant IL-6 to the cell culture, while the growth of EBER2-expressing LCLs was inhibited by a neutralizing anti-IL-6 antibody. These results demonstrate that EBER2, but not EBER1, contributes to efficient B-cell growth transformation. We conclude that EBER1 and EBER2, despite their structural similarity, have different functions in latently infected lymphoblastoid cells.

* Corresponding author. Mailing address: Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, N15W7 Kita-ku, Sapporo 060-0815, Japan. Phone: 81-11-706-5071. Fax: 81-11-706-7540. E-mail: kentaka{at}igm.hokudai.ac.jp

{triangledown} Published ahead of print on 8 August 2007.

Journal of Virology, October 2007, p. 11236-11245, Vol. 81, No. 20
0022-538X/07/$08.00+0     doi:10.1128/JVI.00579-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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