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Journal of Virology, March 2002, p. 2648-2653, Vol. 76, No. 6
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.6.2648-2653.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Human T-Cell Leukemia Virus Type 2 (HTLV-2) Tax Protein Transforms a Rat Fibroblast Cell Line but Less Efficiently than HTLV-1 Tax

Keiichi Endo,1,2 Akira Hirata,1,2 Kousuke Iwai,1 Mamoru Sakurai,1 Masaya Fukushi,1 Masayasu Oie,1 Masaya Higuchi,1 William W. Hall,3 Fumitake Gejyo,2 and Masahiro Fujii1*

Divisions of Virology,1 Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-Dori, Niigata 951-8510, Japan,2 Department of Medical Microbiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Ireland3

Received 7 September 2001/ Accepted 21 November 2001

Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are retroviruses with similar biological properties. Whereas HTLV-1 is the causative agent of an aggressive T-cell leukemia, HTLV-2 has been associated with only a few cases of lymphoproliferative disorders. Tax1 and Tax2 are the transcriptional activators of HTLV-1 and HTLV-2, respectively. Here we show that Tax2 transformed a Rat-1 fibroblast cell line to form colonies in soft agar, but the size and number of the colonies were lower than those of Tax1. Use of a chimeric Tax protein showed that the C-terminal amino acids 300 to 353 were responsible for the high transforming activity of Tax1. Activation of cellular genes by Tax1 through transcription factor NF-{kappa}B is reportedly essential for the transformation of Rat-1 cells. Tax2 also activated the transcription through NF-{kappa}B in Rat-1 cells, and such activity was equivalent to that induced by Tax1. Thus, the high transforming activity of Tax1 is mediated by mechanisms other than NF-{kappa}B activation. Our results showed that Tax2 has a lower transforming activity than Tax1 and suggest that the high transforming activity of Tax1 is involved in the leukemogenic property of HTLV-1.

* Corresponding author. Mailing address: Division of Virology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-Dori, Niigata 951-8510, Japan. Phone: 81 (25) 227-2115. Fax: 81 (25) 227-0763. E-mail: fujiimas{at}med.niigata-u.ac.jp.

Journal of Virology, March 2002, p. 2648-2653, Vol. 76, No. 6
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.6.2648-2653.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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