HTLV-1 infections - PubMed (original) (raw)

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HTLV-1 infections

C R Bangham. J Clin Pathol. 2000 Aug.

Abstract

Human T lymphotropic virus type 1 (HTLV-1) causes disabling and fatal diseases, yet there is no vaccine, no satisfactory treatment, and no means of assessing the risk of disease or prognosis in infected people. Recent research on the molecular virology and immunology of HTLV-1 shows the importance of the host's immune response in reducing the risk of these diseases, and is beginning to explain why some HTLV-1 infected people develop serious illnesses whereas most remain healthy life long carriers of the virus. These findings might be applicable to other persistent virus infections such as human immunodeficiency virus, hepatitis B, and hepatitis C.

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Figures

Figure 1 (A) Distribution of human T lymphotropic virus type 1 (HTLV-1) proviral load in 202 patients with tropical spastic paraparesis (HAM/TSP) and 200 asymptomatic carriers of HTLV-1 (AC) in Kagoshima, southern Japan. 56 The lower limit of detection was one provirus copy/104 peripheral blood mononuclear cells (PBMCs). 56 The median proviral load in patients with HAM/TSP was 16 times greater than in asymptomatic carriers. ND, not determined. (B) The risk of HAM/TSP depends on the proviral load of HTLV-1. The vertical axis shows the risk of HAM/TSP at a given log10 (HTLV-1 proviral load). The risk remains very low until the proviral load reaches 1% PBMCs; above this apparent threshold, the risk of disease rises rapidly with increasing load. The prevalence of HAM/TSP among the seropositive adult population was assumed to be 0.01. 57

Figure 2 Human T lymphotropic virus type 1 (HTLV-1) infection establishes a dynamic equilibrium between virus replication and immune destruction. The infected CD4 positive host cell produces new HTLV-1 virus particles (1), and HTLV-1 derived antigenic peptides complexed with class I and class II human major histocompatibility complex (HLA) proteins on its surface (2). The HTLV-1 virions infect susceptible neighbouring CD4 positive cells. The Tax protein of HTLV-1 acts both as mitogen and antigen, to drive the division of infected CD4 positive and CD8 positive T cells that are specific for Tax (4). The stimulated CD8 positive cytotoxic T cells (CTLs) recognise and kill host cells that express HTLV-1 Tax–HLA protein complexes on the cell surface (5). Tax is not the only HTLV-1 antigen recognised by lymphocytes, but it has a position of special importance because it is the first HTLV-1 protein to be produced, and is a powerful mitogen and antigen.

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