Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation

Autores
Duette, Gabriel; Pereyra Gerber, Federico Pehuén; Rubione, Julia; Pérez, Paula Soledad; Landay, Alan L.; Crowe, Suzanne M.; Liao, Zhaohao; Witwer, Kenneth W.; Holgado, María Pía; Salido, Jimena Patricia; Geffner, Jorge Raúl; Sued, Omar Gustavo; Palmer, Clovis S.; Ostrowski, Matias
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Chronic immune activation and inflammation are hallmarks of HIV-1 infection and a major cause of serious non-AIDS events in HIV-1-infected individuals on antiretroviral treatment (ART). Herein, we show that cytosolic double-stranded DNA (dsDNA) generated in infected CD4 + T cells during the HIV-1 replication cycle promotes the mitochondrial reactive oxygen species (ROS)-dependent stabilization of the transcription factor hypoxia-inducible factor 1α (HIF-1α), which in turn, enhances viral replication. Furthermore, we show that induction of HIF-1α promotes the release of extracellular vesicles (EVs). These EVs foster inflammation by inducing the secretion of gamma interferon by bystander CD4 + T cells and secretion of interleukin 6 (IL-6) and IL-1β by bystander macrophages through an HIF-1α-dependent pathway. Remarkably, EVs obtained from plasma samples from HIV-1-infected individuals also induced HIF-1α activity and inflammation. Overall, this study demonstrates that HIF-1α plays a crucial role in HIV-1 pathogenesis by promoting viral replication and the release of EVs that orchestrate lymphocyte-and macrophage-mediated inflammatory responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) is a very important global pathogen that preferentially targets CD4 + T cells and causes acquired immunodeficiency syndrome (AIDS) if left untreated. Although antiretroviral treatment efficiently suppresses viremia, markers of immune activation and inflammation remain higher in HIV-1-infected patients than in uninfected individuals. The hypoxia-inducible factor 1α (HIF-1α) is a transcription factor that plays a fundamental role in coordinating cellular metabolism and function. Here we show that HIV-1 infection induces HIF-1α activity and that this transcription factor upholds HIV-1 replication. Moreover, we demonstrate that HIF-1α plays a key role in HIV-1-associated inflammation by promoting the release of extracellular vesicles which, in turn, trigger the secretion of inflammatory mediators by noninfected bystander lymphocytes and macrophages. In summary, we identify that the coordinated actions of HIF-1α and extracellular vesicles promote viral replication and inflammation, thus contributing to HIV-1 pathogenesis.
Fil: Duette, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Pereyra Gerber, Federico Pehuén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Rubione, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Pérez, Paula Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Landay, Alan L.. Rush University Medical Center; Estados Unidos
Fil: Crowe, Suzanne M.. Monash University; Australia
Fil: Liao, Zhaohao. Burnet Institute; Australia
Fil: Witwer, Kenneth W.. Alfred Hospital; Australia
Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Salido, Jimena Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Sued, Omar Gustavo. Fundación Huésped; Argentina
Fil: Palmer, Clovis S.. Monash University; Australia
Fil: Ostrowski, Matias. Fundación Huésped; Argentina
Materia
CD4 + T LYMPHOCYTE
EXTRACELLULAR VESICLES
HUMAN IMMUNODEFICIENCY VIRUS
HYPOXIA-INDUCIBLE FACTOR 1 ALPHA
INFLAMMATION
MACROPHAGE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/87735
Acceder
id CONICETDig_0db133475fdf683429c11f220609ebbb
oai_identifier_str oai:ri.conicet.gov.ar:11336/87735
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammationDuette, GabrielPereyra Gerber, Federico PehuénRubione, JuliaPérez, Paula SoledadLanday, Alan L.Crowe, Suzanne M.Liao, ZhaohaoWitwer, Kenneth W.Holgado, María PíaSalido, Jimena PatriciaGeffner, Jorge RaúlSued, Omar GustavoPalmer, Clovis S.Ostrowski, MatiasCD4 + T LYMPHOCYTEEXTRACELLULAR VESICLESHUMAN IMMUNODEFICIENCY VIRUSHYPOXIA-INDUCIBLE FACTOR 1 ALPHAINFLAMMATIONMACROPHAGEhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Chronic immune activation and inflammation are hallmarks of HIV-1 infection and a major cause of serious non-AIDS events in HIV-1-infected individuals on antiretroviral treatment (ART). Herein, we show that cytosolic double-stranded DNA (dsDNA) generated in infected CD4 + T cells during the HIV-1 replication cycle promotes the mitochondrial reactive oxygen species (ROS)-dependent stabilization of the transcription factor hypoxia-inducible factor 1α (HIF-1α), which in turn, enhances viral replication. Furthermore, we show that induction of HIF-1α promotes the release of extracellular vesicles (EVs). These EVs foster inflammation by inducing the secretion of gamma interferon by bystander CD4 + T cells and secretion of interleukin 6 (IL-6) and IL-1β by bystander macrophages through an HIF-1α-dependent pathway. Remarkably, EVs obtained from plasma samples from HIV-1-infected individuals also induced HIF-1α activity and inflammation. Overall, this study demonstrates that HIF-1α plays a crucial role in HIV-1 pathogenesis by promoting viral replication and the release of EVs that orchestrate lymphocyte-and macrophage-mediated inflammatory responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) is a very important global pathogen that preferentially targets CD4 + T cells and causes acquired immunodeficiency syndrome (AIDS) if left untreated. Although antiretroviral treatment efficiently suppresses viremia, markers of immune activation and inflammation remain higher in HIV-1-infected patients than in uninfected individuals. The hypoxia-inducible factor 1α (HIF-1α) is a transcription factor that plays a fundamental role in coordinating cellular metabolism and function. Here we show that HIV-1 infection induces HIF-1α activity and that this transcription factor upholds HIV-1 replication. Moreover, we demonstrate that HIF-1α plays a key role in HIV-1-associated inflammation by promoting the release of extracellular vesicles which, in turn, trigger the secretion of inflammatory mediators by noninfected bystander lymphocytes and macrophages. In summary, we identify that the coordinated actions of HIF-1α and extracellular vesicles promote viral replication and inflammation, thus contributing to HIV-1 pathogenesis.Fil: Duette, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Pereyra Gerber, Federico Pehuén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Rubione, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Pérez, Paula Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Landay, Alan L.. Rush University Medical Center; Estados UnidosFil: Crowe, Suzanne M.. Monash University; AustraliaFil: Liao, Zhaohao. Burnet Institute; AustraliaFil: Witwer, Kenneth W.. Alfred Hospital; AustraliaFil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Salido, Jimena Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Sued, Omar Gustavo. Fundación Huésped; ArgentinaFil: Palmer, Clovis S.. Monash University; AustraliaFil: Ostrowski, Matias. Fundación Huésped; ArgentinaAmerican Society for Microbiology2018-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/87735Duette, Gabriel; Pereyra Gerber, Federico Pehuén; Rubione, Julia; Pérez, Paula Soledad; Landay, Alan L.; et al.; Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation; American Society for Microbiology; mBio; 9; 5; 9-20182161-21292150-7511CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://mbio.asm.org/content/9/5/e00757-18.longinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134101/info:eu-repo/semantics/altIdentifier/doi/10.1128/mBio.00757-18info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:11:24Zoai:ri.conicet.gov.ar:11336/87735instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:11:25.056CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
title Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
spellingShingle Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
Duette, Gabriel
CD4 + T LYMPHOCYTE
EXTRACELLULAR VESICLES
HUMAN IMMUNODEFICIENCY VIRUS
HYPOXIA-INDUCIBLE FACTOR 1 ALPHA
INFLAMMATION
MACROPHAGE
title_short Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
title_full Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
title_fullStr Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
title_full_unstemmed Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
title_sort Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation
dc.creator.none.fl_str_mv Duette, Gabriel
Pereyra Gerber, Federico Pehuén
Rubione, Julia
Pérez, Paula Soledad
Landay, Alan L.
Crowe, Suzanne M.
Liao, Zhaohao
Witwer, Kenneth W.
Holgado, María Pía
Salido, Jimena Patricia
Geffner, Jorge Raúl
Sued, Omar Gustavo
Palmer, Clovis S.
Ostrowski, Matias
author Duette, Gabriel
author_facet Duette, Gabriel
Pereyra Gerber, Federico Pehuén
Rubione, Julia
Pérez, Paula Soledad
Landay, Alan L.
Crowe, Suzanne M.
Liao, Zhaohao
Witwer, Kenneth W.
Holgado, María Pía
Salido, Jimena Patricia
Geffner, Jorge Raúl
Sued, Omar Gustavo
Palmer, Clovis S.
Ostrowski, Matias
author_role author
author2 Pereyra Gerber, Federico Pehuén
Rubione, Julia
Pérez, Paula Soledad
Landay, Alan L.
Crowe, Suzanne M.
Liao, Zhaohao
Witwer, Kenneth W.
Holgado, María Pía
Salido, Jimena Patricia
Geffner, Jorge Raúl
Sued, Omar Gustavo
Palmer, Clovis S.
Ostrowski, Matias
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CD4 + T LYMPHOCYTE
EXTRACELLULAR VESICLES
HUMAN IMMUNODEFICIENCY VIRUS
HYPOXIA-INDUCIBLE FACTOR 1 ALPHA
INFLAMMATION
MACROPHAGE
topic CD4 + T LYMPHOCYTE
EXTRACELLULAR VESICLES
HUMAN IMMUNODEFICIENCY VIRUS
HYPOXIA-INDUCIBLE FACTOR 1 ALPHA
INFLAMMATION
MACROPHAGE
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Chronic immune activation and inflammation are hallmarks of HIV-1 infection and a major cause of serious non-AIDS events in HIV-1-infected individuals on antiretroviral treatment (ART). Herein, we show that cytosolic double-stranded DNA (dsDNA) generated in infected CD4 + T cells during the HIV-1 replication cycle promotes the mitochondrial reactive oxygen species (ROS)-dependent stabilization of the transcription factor hypoxia-inducible factor 1α (HIF-1α), which in turn, enhances viral replication. Furthermore, we show that induction of HIF-1α promotes the release of extracellular vesicles (EVs). These EVs foster inflammation by inducing the secretion of gamma interferon by bystander CD4 + T cells and secretion of interleukin 6 (IL-6) and IL-1β by bystander macrophages through an HIF-1α-dependent pathway. Remarkably, EVs obtained from plasma samples from HIV-1-infected individuals also induced HIF-1α activity and inflammation. Overall, this study demonstrates that HIF-1α plays a crucial role in HIV-1 pathogenesis by promoting viral replication and the release of EVs that orchestrate lymphocyte-and macrophage-mediated inflammatory responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) is a very important global pathogen that preferentially targets CD4 + T cells and causes acquired immunodeficiency syndrome (AIDS) if left untreated. Although antiretroviral treatment efficiently suppresses viremia, markers of immune activation and inflammation remain higher in HIV-1-infected patients than in uninfected individuals. The hypoxia-inducible factor 1α (HIF-1α) is a transcription factor that plays a fundamental role in coordinating cellular metabolism and function. Here we show that HIV-1 infection induces HIF-1α activity and that this transcription factor upholds HIV-1 replication. Moreover, we demonstrate that HIF-1α plays a key role in HIV-1-associated inflammation by promoting the release of extracellular vesicles which, in turn, trigger the secretion of inflammatory mediators by noninfected bystander lymphocytes and macrophages. In summary, we identify that the coordinated actions of HIF-1α and extracellular vesicles promote viral replication and inflammation, thus contributing to HIV-1 pathogenesis.
Fil: Duette, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Pereyra Gerber, Federico Pehuén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Rubione, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Pérez, Paula Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Landay, Alan L.. Rush University Medical Center; Estados Unidos
Fil: Crowe, Suzanne M.. Monash University; Australia
Fil: Liao, Zhaohao. Burnet Institute; Australia
Fil: Witwer, Kenneth W.. Alfred Hospital; Australia
Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Salido, Jimena Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Sued, Omar Gustavo. Fundación Huésped; Argentina
Fil: Palmer, Clovis S.. Monash University; Australia
Fil: Ostrowski, Matias. Fundación Huésped; Argentina
description Chronic immune activation and inflammation are hallmarks of HIV-1 infection and a major cause of serious non-AIDS events in HIV-1-infected individuals on antiretroviral treatment (ART). Herein, we show that cytosolic double-stranded DNA (dsDNA) generated in infected CD4 + T cells during the HIV-1 replication cycle promotes the mitochondrial reactive oxygen species (ROS)-dependent stabilization of the transcription factor hypoxia-inducible factor 1α (HIF-1α), which in turn, enhances viral replication. Furthermore, we show that induction of HIF-1α promotes the release of extracellular vesicles (EVs). These EVs foster inflammation by inducing the secretion of gamma interferon by bystander CD4 + T cells and secretion of interleukin 6 (IL-6) and IL-1β by bystander macrophages through an HIF-1α-dependent pathway. Remarkably, EVs obtained from plasma samples from HIV-1-infected individuals also induced HIF-1α activity and inflammation. Overall, this study demonstrates that HIF-1α plays a crucial role in HIV-1 pathogenesis by promoting viral replication and the release of EVs that orchestrate lymphocyte-and macrophage-mediated inflammatory responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) is a very important global pathogen that preferentially targets CD4 + T cells and causes acquired immunodeficiency syndrome (AIDS) if left untreated. Although antiretroviral treatment efficiently suppresses viremia, markers of immune activation and inflammation remain higher in HIV-1-infected patients than in uninfected individuals. The hypoxia-inducible factor 1α (HIF-1α) is a transcription factor that plays a fundamental role in coordinating cellular metabolism and function. Here we show that HIV-1 infection induces HIF-1α activity and that this transcription factor upholds HIV-1 replication. Moreover, we demonstrate that HIF-1α plays a key role in HIV-1-associated inflammation by promoting the release of extracellular vesicles which, in turn, trigger the secretion of inflammatory mediators by noninfected bystander lymphocytes and macrophages. In summary, we identify that the coordinated actions of HIF-1α and extracellular vesicles promote viral replication and inflammation, thus contributing to HIV-1 pathogenesis.
publishDate 2018
dc.date.none.fl_str_mv 2018-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/87735
Duette, Gabriel; Pereyra Gerber, Federico Pehuén; Rubione, Julia; Pérez, Paula Soledad; Landay, Alan L.; et al.; Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation; American Society for Microbiology; mBio; 9; 5; 9-2018
2161-2129
2150-7511
CONICET Digital
CONICET
url http://hdl.handle.net/11336/87735
identifier_str_mv Duette, Gabriel; Pereyra Gerber, Federico Pehuén; Rubione, Julia; Pérez, Paula Soledad; Landay, Alan L.; et al.; Induction of HIF-1α by HIV-1 infection in CD4 + T cells promotes viral replication and drives extracellular vesicle-mediated inflammation; American Society for Microbiology; mBio; 9; 5; 9-2018
2161-2129
2150-7511
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://mbio.asm.org/content/9/5/e00757-18.long
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134101/
info:eu-repo/semantics/altIdentifier/doi/10.1128/mBio.00757-18
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Society for Microbiology
publisher.none.fl_str_mv American Society for Microbiology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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