Candida albicans delays HIV-1 replication in macrophages

Autores
Rodríguez Rodrígues, Christian Fernando Ariel; Remes Lenicov, Federico; Jancic, Carolina Cristina; Sabatte, Juan Atilio; Cabrini, Mercedes; Ceballos, Ana; Merlotti, Antonela; Gonzalez, Heidi Soledad; Ostrowski, Matias; Geffner, Jorge Raul
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Macrophages are one of the most important HIV-1 target cells. Unlike CD4+ T cells, macrophages are resistant to the cytophatic effect of HIV-1. They are able to produce and harbor the virus for long periods acting as a viral reservoir. Candida albicans (CA) is a commensal fungus that colonizes the portals of HIV-1 entry, such as the vagina and the rectum, and becomes an aggressive pathogen in AIDS patients. In this study, we analyzed the ability of CA to modulate the course of HIV-1 infection in human monocyte-derived macrophages. We found that CA abrogated HIV-1 replication in macrophages when it was evaluated 7 days after virus inoculation. A similar inhibitory effect was observed in monocyte-derived dendritic cells. The analysis of the mechanisms responsible for the inhibition of HIV-1 production in macrophages revealed that CA efficiently sequesters HIV-1 particles avoiding its infectivity. Moreover, by acting on macrophages themselves, CA diminishes their permissibility to HIV-1 infection by reducing the expression of CD4, enhancing the production of the CCR5-interacting chemokines CCL3/MIP-1α, CCL4/MIP-1β, and CCL5/RANTES, and stimulating the production of interferon-α and the restriction factors APOBEC3G, APOBEC3F, and tetherin. Interestingly, abrogation of HIV-1 replication was overcome when the infection of macrophages was evaluated 2-3 weeks after virus inoculation. However, this reactivation of HIV-1 infection could be silenced by CA when added periodically to HIV-1-challenged macrophages. The induction of a silent HIV-1 infection in acrophages at the periphery, where cells are continuously confronted with CA, might help HIV-1 to evade the immune response and to promote resistance to antiretroviral therapy.
Fil: Rodríguez Rodrígues, Christian Fernando Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Jancic, Carolina Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biologia y Medicina Experimental (i); Argentina;
Fil: Sabatte, Juan Atilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Cabrini, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Ceballos, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Merlotti, Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Gonzalez, Heidi Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Ostrowski, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Geffner, Jorge Raul. Consejo Nacional de Investigaciones Científicas y Técnicas . Oficina de Coordinación Administrativa Houssay. Instituto de Inmunologia, Genetica y Metabolismo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Materia
MACROPHAGES
HIV-1
CANDIDA ALBICANS
DENDRITIC CELLS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/1247
Acceder
id CONICETDig_f93246c979d54775676acce39d66260c
oai_identifier_str oai:ri.conicet.gov.ar:11336/1247
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Candida albicans delays HIV-1 replication in macrophagesRodríguez Rodrígues, Christian Fernando ArielRemes Lenicov, FedericoJancic, Carolina CristinaSabatte, Juan AtilioCabrini, MercedesCeballos, AnaMerlotti, AntonelaGonzalez, Heidi SoledadOstrowski, MatiasGeffner, Jorge RaulMACROPHAGESHIV-1CANDIDA ALBICANSDENDRITIC CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Macrophages are one of the most important HIV-1 target cells. Unlike CD4+ T cells, macrophages are resistant to the cytophatic effect of HIV-1. They are able to produce and harbor the virus for long periods acting as a viral reservoir. Candida albicans (CA) is a commensal fungus that colonizes the portals of HIV-1 entry, such as the vagina and the rectum, and becomes an aggressive pathogen in AIDS patients. In this study, we analyzed the ability of CA to modulate the course of HIV-1 infection in human monocyte-derived macrophages. We found that CA abrogated HIV-1 replication in macrophages when it was evaluated 7 days after virus inoculation. A similar inhibitory effect was observed in monocyte-derived dendritic cells. The analysis of the mechanisms responsible for the inhibition of HIV-1 production in macrophages revealed that CA efficiently sequesters HIV-1 particles avoiding its infectivity. Moreover, by acting on macrophages themselves, CA diminishes their permissibility to HIV-1 infection by reducing the expression of CD4, enhancing the production of the CCR5-interacting chemokines CCL3/MIP-1α, CCL4/MIP-1β, and CCL5/RANTES, and stimulating the production of interferon-α and the restriction factors APOBEC3G, APOBEC3F, and tetherin. Interestingly, abrogation of HIV-1 replication was overcome when the infection of macrophages was evaluated 2-3 weeks after virus inoculation. However, this reactivation of HIV-1 infection could be silenced by CA when added periodically to HIV-1-challenged macrophages. The induction of a silent HIV-1 infection in acrophages at the periphery, where cells are continuously confronted with CA, might help HIV-1 to evade the immune response and to promote resistance to antiretroviral therapy.Fil: Rodríguez Rodrígues, Christian Fernando Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Jancic, Carolina Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biologia y Medicina Experimental (i); Argentina;Fil: Sabatte, Juan Atilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Cabrini, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Ceballos, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Merlotti, Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Gonzalez, Heidi Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Ostrowski, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Fil: Geffner, Jorge Raul. Consejo Nacional de Investigaciones Científicas y Técnicas . Oficina de Coordinación Administrativa Houssay. Instituto de Inmunologia, Genetica y Metabolismo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;Public Library Science2013-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/1247Rodriguez Rodrigues, Christian; Remes Lenicov, Federico; Jancic, Carolina; Sabatté, Juan; Cabrini Mercedes; Ceballos, Ana; Merlotti, Antonela; Gonzalez, Heidi; Ostrowski, Matias; Geffner, Jorge; Candida albicans delays HIV-1 replication in macrophages; Public Library Science; Plos One; 23; 2013-8; 72814-72814;1932-6203enginfo:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0072814info:eu-repo/semantics/altIdentifier/url/http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0072814info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:24:20Zoai:ri.conicet.gov.ar:11336/1247instacron: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:34982025-09-10 13:24:20.649CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Candida albicans delays HIV-1 replication in macrophages
title Candida albicans delays HIV-1 replication in macrophages
spellingShingle Candida albicans delays HIV-1 replication in macrophages
Rodríguez Rodrígues, Christian Fernando Ariel
MACROPHAGES
HIV-1
CANDIDA ALBICANS
DENDRITIC CELLS
title_short Candida albicans delays HIV-1 replication in macrophages
title_full Candida albicans delays HIV-1 replication in macrophages
title_fullStr Candida albicans delays HIV-1 replication in macrophages
title_full_unstemmed Candida albicans delays HIV-1 replication in macrophages
title_sort Candida albicans delays HIV-1 replication in macrophages
dc.creator.none.fl_str_mv Rodríguez Rodrígues, Christian Fernando Ariel
Remes Lenicov, Federico
Jancic, Carolina Cristina
Sabatte, Juan Atilio
Cabrini, Mercedes
Ceballos, Ana
Merlotti, Antonela
Gonzalez, Heidi Soledad
Ostrowski, Matias
Geffner, Jorge Raul
author Rodríguez Rodrígues, Christian Fernando Ariel
author_facet Rodríguez Rodrígues, Christian Fernando Ariel
Remes Lenicov, Federico
Jancic, Carolina Cristina
Sabatte, Juan Atilio
Cabrini, Mercedes
Ceballos, Ana
Merlotti, Antonela
Gonzalez, Heidi Soledad
Ostrowski, Matias
Geffner, Jorge Raul
author_role author
author2 Remes Lenicov, Federico
Jancic, Carolina Cristina
Sabatte, Juan Atilio
Cabrini, Mercedes
Ceballos, Ana
Merlotti, Antonela
Gonzalez, Heidi Soledad
Ostrowski, Matias
Geffner, Jorge Raul
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv MACROPHAGES
HIV-1
CANDIDA ALBICANS
DENDRITIC CELLS
topic MACROPHAGES
HIV-1
CANDIDA ALBICANS
DENDRITIC CELLS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Macrophages are one of the most important HIV-1 target cells. Unlike CD4+ T cells, macrophages are resistant to the cytophatic effect of HIV-1. They are able to produce and harbor the virus for long periods acting as a viral reservoir. Candida albicans (CA) is a commensal fungus that colonizes the portals of HIV-1 entry, such as the vagina and the rectum, and becomes an aggressive pathogen in AIDS patients. In this study, we analyzed the ability of CA to modulate the course of HIV-1 infection in human monocyte-derived macrophages. We found that CA abrogated HIV-1 replication in macrophages when it was evaluated 7 days after virus inoculation. A similar inhibitory effect was observed in monocyte-derived dendritic cells. The analysis of the mechanisms responsible for the inhibition of HIV-1 production in macrophages revealed that CA efficiently sequesters HIV-1 particles avoiding its infectivity. Moreover, by acting on macrophages themselves, CA diminishes their permissibility to HIV-1 infection by reducing the expression of CD4, enhancing the production of the CCR5-interacting chemokines CCL3/MIP-1α, CCL4/MIP-1β, and CCL5/RANTES, and stimulating the production of interferon-α and the restriction factors APOBEC3G, APOBEC3F, and tetherin. Interestingly, abrogation of HIV-1 replication was overcome when the infection of macrophages was evaluated 2-3 weeks after virus inoculation. However, this reactivation of HIV-1 infection could be silenced by CA when added periodically to HIV-1-challenged macrophages. The induction of a silent HIV-1 infection in acrophages at the periphery, where cells are continuously confronted with CA, might help HIV-1 to evade the immune response and to promote resistance to antiretroviral therapy.
Fil: Rodríguez Rodrígues, Christian Fernando Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Jancic, Carolina Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biologia y Medicina Experimental (i); Argentina;
Fil: Sabatte, Juan Atilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Cabrini, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Ceballos, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Merlotti, Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Gonzalez, Heidi Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Ostrowski, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
Fil: Geffner, Jorge Raul. Consejo Nacional de Investigaciones Científicas y Técnicas . Oficina de Coordinación Administrativa Houssay. Instituto de Inmunologia, Genetica y Metabolismo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomedicas en Retrovirus y Sida; Argentina;
description Macrophages are one of the most important HIV-1 target cells. Unlike CD4+ T cells, macrophages are resistant to the cytophatic effect of HIV-1. They are able to produce and harbor the virus for long periods acting as a viral reservoir. Candida albicans (CA) is a commensal fungus that colonizes the portals of HIV-1 entry, such as the vagina and the rectum, and becomes an aggressive pathogen in AIDS patients. In this study, we analyzed the ability of CA to modulate the course of HIV-1 infection in human monocyte-derived macrophages. We found that CA abrogated HIV-1 replication in macrophages when it was evaluated 7 days after virus inoculation. A similar inhibitory effect was observed in monocyte-derived dendritic cells. The analysis of the mechanisms responsible for the inhibition of HIV-1 production in macrophages revealed that CA efficiently sequesters HIV-1 particles avoiding its infectivity. Moreover, by acting on macrophages themselves, CA diminishes their permissibility to HIV-1 infection by reducing the expression of CD4, enhancing the production of the CCR5-interacting chemokines CCL3/MIP-1α, CCL4/MIP-1β, and CCL5/RANTES, and stimulating the production of interferon-α and the restriction factors APOBEC3G, APOBEC3F, and tetherin. Interestingly, abrogation of HIV-1 replication was overcome when the infection of macrophages was evaluated 2-3 weeks after virus inoculation. However, this reactivation of HIV-1 infection could be silenced by CA when added periodically to HIV-1-challenged macrophages. The induction of a silent HIV-1 infection in acrophages at the periphery, where cells are continuously confronted with CA, might help HIV-1 to evade the immune response and to promote resistance to antiretroviral therapy.
publishDate 2013
dc.date.none.fl_str_mv 2013-08
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/11336/1247
Rodriguez Rodrigues, Christian; Remes Lenicov, Federico; Jancic, Carolina; Sabatté, Juan; Cabrini Mercedes; Ceballos, Ana; Merlotti, Antonela; Gonzalez, Heidi; Ostrowski, Matias; Geffner, Jorge; Candida albicans delays HIV-1 replication in macrophages; Public Library Science; Plos One; 23; 2013-8; 72814-72814;
1932-6203
url http://hdl.handle.net/11336/1247
identifier_str_mv Rodriguez Rodrigues, Christian; Remes Lenicov, Federico; Jancic, Carolina; Sabatté, Juan; Cabrini Mercedes; Ceballos, Ana; Merlotti, Antonela; Gonzalez, Heidi; Ostrowski, Matias; Geffner, Jorge; Candida albicans delays HIV-1 replication in macrophages; Public Library Science; Plos One; 23; 2013-8; 72814-72814;
1932-6203
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0072814
info:eu-repo/semantics/altIdentifier/url/http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0072814
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Public Library Science
publisher.none.fl_str_mv Public Library Science
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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score 12.48226

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