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Microbiology and Molecular Biology Reviews, June 1999, p. 308-333, Vol. 63, No. 2
1092-2172/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Mechanisms of T-Cell Activation by Human T-Cell Lymphotropic Virus Type I

Per Höllsberg*

Department of Medical Microbiology and Immunology, Aarhus University, Aarhus, Denmark

The interactions between human T-cell lymphotropic virus type I (HTLV-I) and the cellular immune system can be divided into viral interference with functions of the infected host T cell and the subsequent interactions between the infected T cell and the cellular immune system. HTLV-I-mediated activation of the infected host T cell is induced primarily by the viral protein Tax, which influences transcriptional activation, signal transduction pathways, cell cycle control, and apoptosis. These properties of Tax may well explain the ability of HTLV-I to immortalize T cells. It is not clear, though, how HTLV-I induces T-cell transformation (interleukin-2 [IL-2] independence). Recent evidence suggests that Tax may promote the G1- to S-phase transition, although this may involve additional proteins. A role for other viral proteins that may constitutively activate the IL-2 receptor pathway has also been suggested. By virtue of their activated state, HTLV-I-infected T cells can nonspecifically activate resting, uninfected T cells via virus-mediated upregulation of adhesion molecules. This may favor viral dissemination. Moreover, the induction of a remarkably high frequency of antiviral CD8+ T cells does not appear to eliminate the infection. Indeed, individuals with a high frequency of virus-specific CD8+ T cells have a high viral load, indicating a state of chronic immune system stimulation. Thus, while an activated immune system is needed to eradicate the infection, the spread of the HTLV-I is also accelerated under these conditions. A detailed knowledge of the molecular interactions between virus-specific CD8+ T cells and immunodominant viral epitopes holds promise for the development of specific antiviral therapy.

* Mailing address: Division of Virology, Department of Medical Microbiology and Immunology, Bartholin Building, Aarhus University, DK-8000 Aarhus, Denmark. Phone: 45 8942 1772. Fax: 45 8619 6128. E-mail: ph{at}microbiology.au.dk.

Microbiology and Molecular Biology Reviews, June 1999, p. 308-333, Vol. 63, No. 2
1092-2172/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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Copyright © 1999 by the American Society for Microbiology. All rights reserved.