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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1386-1392
Abundant Tax protein expression in CD4+ T cells infected with
human T-cell lymphotropic virus type I (HTLV-I) is prevented by
cytotoxic T lymphocytes
Emmanuel Hanon,
Sarah Hall,
Graham P. Taylor,
Mineki Saito,
Ricardo Davis,
Yuetsu Tanaka,
Koichiro Usuku,
Mitsuhiro Osame,
Jonathan N. Weber, and
Charles R. M. Bangham
From the Department of Immunology and Genito-Urinary Medicine and
Communicable Diseases, Imperial College School of Medicine, St Mary's
Campus, London, United Kingdom; Department of Infectious Disease and
Immunology, Okinawa-Asia Research Center of Medical Science, Faculty of
Medicine, University of The Ryukyus, Nishihara, Okinawa, Japan; and
Department of Medical Informatics and Third Department of Internal
Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
The role of the cellular immune response in human T-cell leukemia
virus type I (HTLV-I) infection is not fully understood. A persistently
activated cytotoxic T lymphocyte (CTL) response to HTLV-I is found in
the majority of infected individuals. However, it remains unclear
whether this CTL response is protective or causes tissue damage. In
addition, several observations paradoxically suggest that HTLV-I is
transcriptionally silent in most infected cells and, therefore, not
detectable by virus-specific CTLs. With the use of a new flow
cytometric procedure, we show here that a high proportion of naturally
infected CD4+ peripheral blood mononuclear cells (PBMC) (between 10%
and 80%) are capable of expressing Tax, the immunodominant target
antigen recognized by virus-specific CTLs. Furthermore, we provide
direct evidence that autologous CD8+ T cells rapidly kill CD4+
cells naturally infected with HTLV-I and expressing Tax in vitro by a
perforin-dependent mechanism. Consistent with these observations, we
observed a significant negative correlation between the frequency of
Tax11-19-specific CD8+ T cells and the percentage of
CD4+ T cells in peripheral blood of patients infected with HTLV-I.
Those results are in accordance with the view that virus-specific CTLs
participate in a highly efficient immune surveillance mechanism that
persistently destroys Tax-expressing HTLV-I-infected CD4+ T cells in vivo.
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