Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity

<p>Abstract</p> <p>Background</p> <p>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. Other factors might thus importantly contribute in increasing infection by HTLV-I. G...

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Main Authors: Sato Sachiko, Tremblay Michel J, Vargas Amandine, Ouellet Michel, Pelletier Isabelle, Gauthier Sonia, Barbeau Benoit
Format: Article
Language:English
Published: BMC 2008-11-01
Series:Retrovirology
Online Access:http://www.retrovirology.com/content/5/1/105
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author Sato Sachiko
Tremblay Michel J
Vargas Amandine
Ouellet Michel
Pelletier Isabelle
Gauthier Sonia
Barbeau Benoit
author_facet Sato Sachiko
Tremblay Michel J
Vargas Amandine
Ouellet Michel
Pelletier Isabelle
Gauthier Sonia
Barbeau Benoit
author_sort Sato Sachiko
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p>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. 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.</p> <p>Results</p> <p>Herein, 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.</p> <p>Conclusion</p> <p>These 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.</p>
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spelling doaj.art-1031e1608e5f46b08e593544ec9944302022-12-22T02:14:32ZengBMCRetrovirology1742-46902008-11-015110510.1186/1742-4690-5-105Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivitySato SachikoTremblay Michel JVargas AmandineOuellet MichelPelletier IsabelleGauthier SoniaBarbeau Benoit<p>Abstract</p> <p>Background</p> <p>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. 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.</p> <p>Results</p> <p>Herein, 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.</p> <p>Conclusion</p> <p>These 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.</p>http://www.retrovirology.com/content/5/1/105
spellingShingle Sato Sachiko
Tremblay Michel J
Vargas Amandine
Ouellet Michel
Pelletier Isabelle
Gauthier Sonia
Barbeau Benoit
Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
Retrovirology
title Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
title_full Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
title_fullStr Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
title_full_unstemmed Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
title_short Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity
title_sort induction of galectin 1 expression by htlv i tax and its impact on htlv i infectivity
url http://www.retrovirology.com/content/5/1/105
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