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Journal of Virology, August 2006, p. 7375-7381, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00230-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Reduction of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Proviral Loads in Rats Orally Infected with HTLV-1 by Reimmunization with HTLV-1-Infected Cells

Kazuya Komori,1,2,{dagger} Atsuhiko Hasegawa,1,3,{dagger} Kiyoshi Kurihara,1 Takayuki Honda,1 Hiroo Yokozeki,2 Takao Masuda,1 and Mari Kannagi1*

Department of Immunotherapeutics,1 Department of Dermatology, Tokyo Medical and Dental University Graduate School, Tokyo 113-8519, Japan,2 Division of Immunology, Tulane National Primate Research Center, Tulane, Louisiana 704333

Received 1 February 2006/ Accepted 30 April 2006

Human T-cell leukemia virus type 1 (HTLV-1) persistently infects humans, and the proviral loads that persist in vivo vary widely among individuals. Elevation in the proviral load is associated with serious HTLV-1-mediated diseases, such as adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis. However, it remains controversial whether HTLV-1-specific T-cell immunity can control HTLV-1 in vivo. We previously reported that orally HTLV-1-infected rats showed insufficient HTLV-1-specific T-cell immunity that coincided with elevated levels of the HTLV-1 proviral load. In the present study, we found that individual HTLV-1 proviral loads established in low-responding hosts could be reduced by the restoration of HTLV-1-specific T-cell responses. Despite the T-cell unresponsiveness for HTLV-1 in orally infected rats, an allogeneic mixed lymphocyte reaction in the splenocytes and a contact hypersensitivity response in the skin of these rats were comparable with those of naive rats. HTLV-1-specific T-cell response in orally HTLV-1-infected rats could be restored by subcutaneous reimmunization with mitomycin C (MMC)-treated syngeneic HTLV-1-transformed cells. The reimmunized rats exhibited lower proviral loads than untreated orally infected rats. We also confirmed that the proviral loads in orally infected rats decreased after reimmunization in the same hosts. Similar T-cell immune conversion could be reproduced in orally HTLV-1-infected rats by subcutaneous inoculation with MMC-treated primary T cells from syngeneic orally HTLV-1-infected rats. The present results indicate that, although HTLV-1-specific T-cell unresponsiveness is an underlying risk factor for the propagation of HTLV-1-infected cells in vivo, the risk may potentially be reduced by reimmunization, for which autologous HTLV-1-infected cells are a candidate immunogen.

* Corresponding author. Mailing address: Department of Immunotherapeutics, Faculty of Medicine, Tokyo Medical and Dental University, Medical Research Division, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. Phone: 81-3-5803-5798. Fax: 81-3-5803-0235. E-mail: kann.impt{at}tmd.ac.jp.

{dagger} K.K. and A.H. contributed equally to this study.

Journal of Virology, August 2006, p. 7375-7381, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.00230-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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