HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells

Introduction: Current antiretroviral therapy (ART) for HIV infection reduces plasma viral loads to undetectable levels and has increased the life expectancy of people with HIV (PWH). However, this increased lifespan is accompanied by signs of accelerated aging and a higher prevalence of age-related...

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Autores: Casanova Güell, Víctor, Rodríguez-Agustín, Andrea, Ayala-Suárez, Rubén, Moraga López, Elisa, Maleno, María José, Mallolas Masferrer, Josep, Martínez Chamorro, Esteban José, Sánchez-Palomino, Sonsoles, Miró Meda, José M. (José María), 1956-, Alcamí, José, Climent Vidal, Núria
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/223671
Acceso en línea:https://hdl.handle.net/2445/223671
Access Level:acceso abierto
Palabra clave:Sida
VIH (Virus)
Envelliment
Metabolisme cel·lular
AIDS (Disease)
HIV (Viruses)
Aging
Cell metabolism
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spelling HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cellsCasanova Güell, VíctorRodríguez-Agustín, AndreaAyala-Suárez, RubénMoraga López, ElisaMaleno, María JoséMallolas Masferrer, JosepMartínez Chamorro, Esteban JoséSánchez-Palomino, SonsolesMiró Meda, José M. (José María), 1956-Alcamí, JoséCliment Vidal, NúriaSidaVIH (Virus)EnvellimentMetabolisme cel·lularAIDS (Disease)HIV (Viruses)AgingCell metabolismIntroduction: Current antiretroviral therapy (ART) for HIV infection reduces plasma viral loads to undetectable levels and has increased the life expectancy of people with HIV (PWH). However, this increased lifespan is accompanied by signs of accelerated aging and a higher prevalence of age-related comorbidities. Tat (Trans-Activator of Transcription) is a key protein for viral replication and pathogenesis. Tat is encoded by 2 exons, with the full-length Tat ranging from 86 to 101 aa (Tat101). Introducing a stop codon in position 73 generates a 1 exon, synthetic 72aa Tat (Tat72). Intracellular, full-length Tat activates the NF-κB pro-inflammatory pathway and increases antiapoptotic signals and ROS generation. These effects may initiate a cellular senescence program, characterized by cell cycle arrest, altered cell metabolism, and increased senescence-associated secretory phenotype (SASP) mediator release However, the precise role of HIV-Tat in inducing a cellular senescence program in CD4+ T-cells is currently unknown. Methods: Jurkat Tetoff cell lines stably transfected with Tat72, Tat101, or an empty vector were used. Flow cytometry and RT-qPCR were used to address senescence biomarkers, and 105 mediators were assessed in cell supernatants with an antibody-based membrane array. Key results obtained in Jurkat-Tat cells were addressed in primary, resting CD4+ T-cells by transient electroporation of HIV-Tat-FLAG plasmid DNA. Results: In the Jurkat cell model, expression of Tat101 increased the levels of the senescence biomarkers BCL-2, CD87, and p21, and increased the release of sCD30, PDGF-AA, and sCD31, among other factors. Tat101 upregulated CD30 and CD31 co-expression in the Jurkat cell surface, distinguishing these cells from Tat72 and Tetoff Jurkats. The percentage of p21+, p16+, and γ-H2AX+ cells were higher in Tat-expressing CD4+ T-cells, detected as a FLAG+ population compared to their FLAG- (Tat negative) counterparts. Increased levels of sCD31 and sCD26 were also detected in electroporated CD4+ T-cell supernatants. Discussion: Intracellular, full-length HIV-Tat expression increases several senescence biomarkers in Jurkat and CD4+ T-cells, and SASP/Aging mediators in cell supernatants. Intracellular HIV-Tat may initiate a cellular senescence program, contributing to the premature aging phenotype observed in PWH.Frontiers Media2025202520252025info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion16 p.application/pdfhttps://hdl.handle.net/2445/223671Articles publicats en revistes (Medicina)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReproducció del document publicat a: https://doi.org/10.3389/fimmu.2025.1568762Frontiers in Immunology, 2025, num.1568762https://doi.org/10.3389/fimmu.2025.1568762cc-by (c) Casanova, Víctor et al., 2025http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:recercat.cat:2445/2236712026-05-29T05:05:01Z
dc.title.none.fl_str_mv HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
title HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
spellingShingle HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
Casanova Güell, Víctor
Sida
VIH (Virus)
Envelliment
Metabolisme cel·lular
AIDS (Disease)
HIV (Viruses)
Aging
Cell metabolism
title_short HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
title_full HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
title_fullStr HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
title_full_unstemmed HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
title_sort HIV-Tat upregulates the expression of senescence biomarkers in CD4+T-cells
dc.creator.none.fl_str_mv Casanova Güell, Víctor
Rodríguez-Agustín, Andrea
Ayala-Suárez, Rubén
Moraga López, Elisa
Maleno, María José
Mallolas Masferrer, Josep
Martínez Chamorro, Esteban José
Sánchez-Palomino, Sonsoles
Miró Meda, José M. (José María), 1956-
Alcamí, José
Climent Vidal, Núria
author Casanova Güell, Víctor
author_facet Casanova Güell, Víctor
Rodríguez-Agustín, Andrea
Ayala-Suárez, Rubén
Moraga López, Elisa
Maleno, María José
Mallolas Masferrer, Josep
Martínez Chamorro, Esteban José
Sánchez-Palomino, Sonsoles
Miró Meda, José M. (José María), 1956-
Alcamí, José
Climent Vidal, Núria
author_role author
author2 Rodríguez-Agustín, Andrea
Ayala-Suárez, Rubén
Moraga López, Elisa
Maleno, María José
Mallolas Masferrer, Josep
Martínez Chamorro, Esteban José
Sánchez-Palomino, Sonsoles
Miró Meda, José M. (José María), 1956-
Alcamí, José
Climent Vidal, Núria
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Sida
VIH (Virus)
Envelliment
Metabolisme cel·lular
AIDS (Disease)
HIV (Viruses)
Aging
Cell metabolism
topic Sida
VIH (Virus)
Envelliment
Metabolisme cel·lular
AIDS (Disease)
HIV (Viruses)
Aging
Cell metabolism
description Introduction: Current antiretroviral therapy (ART) for HIV infection reduces plasma viral loads to undetectable levels and has increased the life expectancy of people with HIV (PWH). However, this increased lifespan is accompanied by signs of accelerated aging and a higher prevalence of age-related comorbidities. Tat (Trans-Activator of Transcription) is a key protein for viral replication and pathogenesis. Tat is encoded by 2 exons, with the full-length Tat ranging from 86 to 101 aa (Tat101). Introducing a stop codon in position 73 generates a 1 exon, synthetic 72aa Tat (Tat72). Intracellular, full-length Tat activates the NF-κB pro-inflammatory pathway and increases antiapoptotic signals and ROS generation. These effects may initiate a cellular senescence program, characterized by cell cycle arrest, altered cell metabolism, and increased senescence-associated secretory phenotype (SASP) mediator release However, the precise role of HIV-Tat in inducing a cellular senescence program in CD4+ T-cells is currently unknown. Methods: Jurkat Tetoff cell lines stably transfected with Tat72, Tat101, or an empty vector were used. Flow cytometry and RT-qPCR were used to address senescence biomarkers, and 105 mediators were assessed in cell supernatants with an antibody-based membrane array. Key results obtained in Jurkat-Tat cells were addressed in primary, resting CD4+ T-cells by transient electroporation of HIV-Tat-FLAG plasmid DNA. Results: In the Jurkat cell model, expression of Tat101 increased the levels of the senescence biomarkers BCL-2, CD87, and p21, and increased the release of sCD30, PDGF-AA, and sCD31, among other factors. Tat101 upregulated CD30 and CD31 co-expression in the Jurkat cell surface, distinguishing these cells from Tat72 and Tetoff Jurkats. The percentage of p21+, p16+, and γ-H2AX+ cells were higher in Tat-expressing CD4+ T-cells, detected as a FLAG+ population compared to their FLAG- (Tat negative) counterparts. Increased levels of sCD31 and sCD26 were also detected in electroporated CD4+ T-cell supernatants. Discussion: Intracellular, full-length HIV-Tat expression increases several senescence biomarkers in Jurkat and CD4+ T-cells, and SASP/Aging mediators in cell supernatants. Intracellular HIV-Tat may initiate a cellular senescence program, contributing to the premature aging phenotype observed in PWH.
publishDate 2025
dc.date.none.fl_str_mv 2025
2025
2025
2025
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/223671
url https://hdl.handle.net/2445/223671
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2025.1568762
Frontiers in Immunology, 2025, num.1568762
https://doi.org/10.3389/fimmu.2025.1568762
dc.rights.none.fl_str_mv cc-by (c) Casanova, Víctor et al., 2025
http://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by (c) Casanova, Víctor et al., 2025
http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 16 p.
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
dc.source.none.fl_str_mv Articles publicats en revistes (Medicina)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
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repository.mail.fl_str_mv
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