Abstract
BackgroundCell-free Human T-cell Leukemia Virus type I (HTLV-I) virions are poorly infectious and cell-to-cell contact is often required to achieve infection. Other factors might thus importantly contribute in increasing infection by HTLV-I. Galectin-1 is a galactoside-binding lectin which is secreted by activated T lymphocytes. Several functions have been attributed to this protein including its capacity to increase cell-to-cell adhesion. Based on previous studies, we postulated that this protein could also accentuate HTLV-I infection.ResultsHerein, we demonstrate that galectin-1 expression and release are higher in HTLV-I-infected T cells in comparison to uninfected T cells. Furthermore, galectin-1 expression was activated in various cell lines expressing the wild type viral Tax protein while this induction was minimal upon expression of NF-κB activation-defective TaxM22. Cotransfection of these Tax expression vectors with galectin-1 promoter-driven luciferase constructs confirmed that Tax upregulated galectin-1 promoter activity. However, a NF-κB-independent mechanism was strongly favoured in this induction of galectin-1 expression as no activation of the promoter was apparent in Jurkat cells treated with known NF-κB activators. Using HTLV-I envelope pseudotyped HIV-1 virions, galectin-1 was shown to increase infectivity. In addition, a co-culture assay with HTLV-I-infected cells also indicated an increase in cell fusion upon addition of galectin-1. This effect was not mediated by factors present in the supernatant of the HTLV-I-infected cells.ConclusionThese data suggest that HTLV-I Tax increases galectin-1 expression and that this modulation could play an important role in HTLV-I infection by stabilizing both cell-to-cell and virus-cell interactions.
Highlights
Cell-free Human T-cell Leukemia Virus type I (HTLV-I) virions are poorly infectious and cell-to-cell contact is often required to achieve infection
Galectin-1 is more strongly expressed in HTLV-I-infected T cells than in non-infected T cells Previous studies have suggested that expression of various genes are positively modulated in HTLV-I-infected cells [19,57]
In order to determine whether galectin-1 expression is altered in HTLV-I-infected cells, RT-PCR experiments were performed to compare the level of galectin-1 gene expression between non infected human T cells and HTLV-I-infected human T cells
Summary
Cell-free Human T-cell Leukemia Virus type I (HTLV-I) virions are poorly infectious and cell-to-cell contact is often required to achieve infection. Several functions have been attributed to this protein including its capacity to increase cell-to-cell adhesion. HTLV-I is transmitted between individuals by the transfer of infected lymphocytes and is thought to require repeated contacts as only one out of 1 × 105 to 1 × 106 viruses is infectious [79]. The cellular ICAM-1 protein has been established as a potential inducer of microtubule reorganization, the viral Tax protein has been shown to be active in this process [12,13]
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