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Journal of Virology, March 2003, p. 2956-2963, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2956-2963.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Expansion of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Reservoir in Orally Infected Rats: Inverse Correlation with HTLV-1-Specific Cellular Immune Response

Atsuhiko Hasegawa, Takashi Ohashi, Shino Hanabuchi, Hirotomo Kato, Fumiyo Takemura, Takao Masuda, and Mari Kannagi*

Department of Immunotherapeutics, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8519, Japan

Received 26 August 2002/ Accepted 26 November 2002

Adult T-cell leukemia (ATL) occurs in a small population of human T-cell leukemia virus type 1 (HTLV-1)-infected individuals. Although the critical risk factor for ATL development is not clear, it has been noted that ATL is incidentally associated with mother-to-child infection, elevated proviral loads, and weakness in HTLV-1-specific T-cell immune responses. In the present study, using a rat system, we investigated the relationships among the following conditions: primary HTLV-1 infection, a persistent HTLV-1 load, and host HTLV-1-specific immunity. We found that the persistent HTLV-1 load in orally infected rats was significantly greater than that in intraperitoneally infected rats. Even after inoculation with only 50 infected cells, a persistent viral load built up to considerable levels in some orally infected rats but not in intraperitoneally infected rats. In contrast, HTLV-1-specific cellular immune responses were markedly impaired in orally infected rats. As a result, a persistent viral load was inversely correlated with levels of virus-specific T-cell responses in these rats. Otherwise very weak HTLV-1-specific cellular immune responses in orally infected rats were markedly augmented after subcutaneous reimmunization with infected syngeneic rat cells. These findings suggest that HTLV-1-specific immune unresponsiveness associated with oral HTLV-1 infection may be a potential risk factor for development of ATL, allowing expansion of the infected cell reservoir in vivo, but could be overcome with immunological strategies.

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

Journal of Virology, March 2003, p. 2956-2963, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2956-2963.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Komori, K., Hasegawa, A., Kurihara, K., Honda, T., Yokozeki, H., Masuda, T., Kannagi, M. (2006). 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.. J. Virol. 80: 7375-7381 [Abstract] [Full Text]  
  • Bangham, C. R. M. (2003). The immune control and cell-to-cell spread of human T-lymphotropic virus type 1. J. Gen. Virol. 84: 3177-3189 [Abstract] [Full Text]  


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