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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Format: | Article |
Language: | English |
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BMC
2008-11-01
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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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institution | Directory Open Access Journal |
issn | 1742-4690 |
language | English |
last_indexed | 2024-04-14T03:40:10Z |
publishDate | 2008-11-01 |
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series | Retrovirology |
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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