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Abstract
Background The HTLV-1 proviral load set point is the strongest correlate of the inflammatory and malignant diseases associated with HTLV-1. This set point appears to be determined by an equilibrium between virus-driven proliferation and CTL-mediated killing of HTLV-1-infected T cells. However, we do not know what determines the number, the abundance or the pathogenic potential of HTLV-1-infected T cell clones. In addition, the contribution of de novo infection to HTLV-1 persistence in the host remains uncertain. We hypothesize that the genomic integration site (IS) of the HTLV-1 provirus determines the pattern and intensity of spontaneous proviral expression; the viral gene products in turn determine the rate of proliferation of the infected cells, and the rate of CTL-mediated killing. We aim to identify the factors that determine the integration site targeting, expression and abundance of the HTLV-1 provirus in natural infection.
Highlights
The HTLV-1 proviral load set point is the strongest correlate of the inflammatory and malignant diseases associated with HTLV-1
We hypothesize that the genomic integration site (IS) of the HTLV-1 provirus determines the pattern and intensity of spontaneous proviral expression; the viral gene products in turn determine the rate of proliferation of the infected cells, and the rate of CTL-mediated killing
Materials and methods We developed a novel protocol [1,2] for high-throughput mapping and accurate quantification of proviral integration sites in the host genome in fresh uncultured peripheral blood mononuclear cells from individuals with different clinical manifestations of HTLV-1 infection
Summary
The HTLV-1 proviral load set point is the strongest correlate of the inflammatory and malignant diseases associated with HTLV-1. This set point appears to be determined by an equilibrium between virus-driven proliferation and CTL-mediated killing of HTLV-1-infected T cells. We do not know what determines the number, the abundance or the pathogenic potential of HTLV-1-infected T cell clones. We hypothesize that the genomic integration site (IS) of the HTLV-1 provirus determines the pattern and intensity of spontaneous proviral expression; the viral gene products in turn determine the rate of proliferation of the infected cells, and the rate of CTL-mediated killing. We aim to identify the factors that determine the integration site targeting, expression and abundance of the HTLV-1 provirus in natural infection
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