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Journal of Virology, April 2004, p. 3984-3993, Vol. 78, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.8.3984-3993.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus Nuclear Antigen Leader Protein Induces Expression of Thymus- and Activation-Regulated Chemokine in B Cells

Mikiko Kanamori,1,2 Shinya Watanabe,3 Reiko Honma,3,4 Masayuki Kuroda,5 Shosuke Imai,5 Kenzo Takada,6 Naoki Yamamoto,2 Yukihiro Nishiyama,1 and Yasushi Kawaguchi1,7*

Department of Virology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550,1 PRESTO, Japan Science and Technology Agency, Kawaguchi, Saitama, 332-0012,7 Department of Molecular Virology, Tokyo Medical and Dental University School of Medicine, Bunkyo-ku, Tokyo 113-8519,2 Division of Cancer Genomics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639,3 The Japan Biological Informatics Consortium, Chuo-ku, Tokyo 104-0032,4 Department of Molecular Microbiology and Infections Program of Bio-signaling and Infection Control, Kochi Medical School, Kochi 783-8505,5 Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan6

Received 28 August 2003/ Accepted 11 December 2003

Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP) plays a critical role in transformation of primary B lymphocytes to continuously proliferating lymphoblastoid cell lines (LCLs). To identify cellular genes in B cells whose expression is regulated by EBNA-LP, we performed microarray expression profiling on an EBV-negative human B-cell line, BJAB cells, that were transduced by a retroviral vector expressing the EBV EBNA-LP (BJAB-LP cells) and on BJAB cells that were transduced with a control vector (BJAB-vec cells). Microarray analysis led to the identification of a cellular gene encoding the CC chemokine TARC as a novel target gene that was induced by EBNA-LP. The levels of TARC mRNA expression and TARC secretion were significantly up-regulated in BJAB-LP compared with BJAB-vec cells. Induction of TARC was also observed when a subline of BJAB cells was converted by a recombinant EBV. Among the EBV-infected B-cell lines with the latency III phenotype that were tested, the LCLs especially secreted significantly high levels of TARC. The level of TARC secretion appeared to correlate with the level of full-length EBNA-LP expression. These results indicate that EBV infection induces TARC expression in B cells and that EBNA-LP is one of the viral gene products responsible for the induction.

* Corresponding author. Mailing address: Department of Virology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Phone: 81-52-744-2207. Fax: 81-52-744-2452. E-mail: ykawagu{at}med.nagoya-u.ac.jp.

Journal of Virology, April 2004, p. 3984-3993, Vol. 78, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.8.3984-3993.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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