Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi

Autores
Andreani, Guadalupe; Celentano Stanic, Ana Maria Luisa Micaela; Solana, Maria Elisa; Cazorla, Silvia Ines; Malchiodi, Emilio Luis; Martinez Peralta, Liliana A.; Dolcini, Guillermina Laura
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: Cells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date. Methodology/Principal Findings: By using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p,0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p,0.001), T. cruzi-HIV (.99%) being stronger than HIV-T.cruzi (,90% for BaL and ,85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p,0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p,0.05). Thus, T. cruzi inhibits viral postintegration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ,60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p,0.01). Conclusions/Significance: Our study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.
Fil: Andreani, Guadalupe. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Celentano Stanic, Ana Maria Luisa Micaela. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Solana, Maria Elisa. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cazorla, Silvia Ines. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Malchiodi, Emilio Luis. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología. Cátedra de Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Martinez Peralta, Liliana A.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Dolcini, Guillermina Laura. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
HIV
TRYPANOSOMA CRUZI
HUMAN MACROPHAGES
COINFECTION
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:11336/82016
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/82016
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruziAndreani, GuadalupeCelentano Stanic, Ana Maria Luisa MicaelaSolana, Maria ElisaCazorla, Silvia InesMalchiodi, Emilio LuisMartinez Peralta, Liliana A.Dolcini, Guillermina LauraHIVTRYPANOSOMA CRUZIHUMAN MACROPHAGESCOINFECTIONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Background: Cells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date. Methodology/Principal Findings: By using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p,0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p,0.001), T. cruzi-HIV (.99%) being stronger than HIV-T.cruzi (,90% for BaL and ,85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p,0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p,0.05). Thus, T. cruzi inhibits viral postintegration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ,60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p,0.01). Conclusions/Significance: Our study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.Fil: Andreani, Guadalupe. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Celentano Stanic, Ana Maria Luisa Micaela. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaFil: Solana, Maria Elisa. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cazorla, Silvia Ines. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Malchiodi, Emilio Luis. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología. Cátedra de Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Martinez Peralta, Liliana A.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Dolcini, Guillermina Laura. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaPublic Library of Science2009-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/82016Andreani, Guadalupe; Celentano Stanic, Ana Maria Luisa Micaela; Solana, Maria Elisa; Cazorla, Silvia Ines; Malchiodi, Emilio Luis; et al.; Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi; Public Library of Science; Plos One; 4; 12; 12-2009; 1-13; e82461932-6203CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008246info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0008246info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:35:32Zoai:ri.conicet.gov.ar:11336/82016instacron: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:34982025-10-15 14:35:33.272CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
title Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
spellingShingle Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
Andreani, Guadalupe
HIV
TRYPANOSOMA CRUZI
HUMAN MACROPHAGES
COINFECTION
title_short Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
title_full Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
title_fullStr Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
title_full_unstemmed Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
title_sort Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi
dc.creator.none.fl_str_mv Andreani, Guadalupe
Celentano Stanic, Ana Maria Luisa Micaela
Solana, Maria Elisa
Cazorla, Silvia Ines
Malchiodi, Emilio Luis
Martinez Peralta, Liliana A.
Dolcini, Guillermina Laura
author Andreani, Guadalupe
author_facet Andreani, Guadalupe
Celentano Stanic, Ana Maria Luisa Micaela
Solana, Maria Elisa
Cazorla, Silvia Ines
Malchiodi, Emilio Luis
Martinez Peralta, Liliana A.
Dolcini, Guillermina Laura
author_role author
author2 Celentano Stanic, Ana Maria Luisa Micaela
Solana, Maria Elisa
Cazorla, Silvia Ines
Malchiodi, Emilio Luis
Martinez Peralta, Liliana A.
Dolcini, Guillermina Laura
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv HIV
TRYPANOSOMA CRUZI
HUMAN MACROPHAGES
COINFECTION
topic HIV
TRYPANOSOMA CRUZI
HUMAN MACROPHAGES
COINFECTION
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Background: Cells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date. Methodology/Principal Findings: By using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p,0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p,0.001), T. cruzi-HIV (.99%) being stronger than HIV-T.cruzi (,90% for BaL and ,85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p,0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p,0.05). Thus, T. cruzi inhibits viral postintegration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ,60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p,0.01). Conclusions/Significance: Our study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.
Fil: Andreani, Guadalupe. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Celentano Stanic, Ana Maria Luisa Micaela. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Solana, Maria Elisa. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cazorla, Silvia Ines. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Malchiodi, Emilio Luis. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología. Cátedra de Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Martinez Peralta, Liliana A.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Dolcini, Guillermina Laura. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Centro Nacional de Referencia para el Sida; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description Background: Cells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date. Methodology/Principal Findings: By using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p,0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p,0.001), T. cruzi-HIV (.99%) being stronger than HIV-T.cruzi (,90% for BaL and ,85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p,0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p,0.05). Thus, T. cruzi inhibits viral postintegration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ,60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p,0.01). Conclusions/Significance: Our study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.
publishDate 2009
dc.date.none.fl_str_mv 2009-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/82016
Andreani, Guadalupe; Celentano Stanic, Ana Maria Luisa Micaela; Solana, Maria Elisa; Cazorla, Silvia Ines; Malchiodi, Emilio Luis; et al.; Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi; Public Library of Science; Plos One; 4; 12; 12-2009; 1-13; e8246
1932-6203
CONICET Digital
CONICET
url http://hdl.handle.net/11336/82016
identifier_str_mv Andreani, Guadalupe; Celentano Stanic, Ana Maria Luisa Micaela; Solana, Maria Elisa; Cazorla, Silvia Ines; Malchiodi, Emilio Luis; et al.; Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi; Public Library of Science; Plos One; 4; 12; 12-2009; 1-13; e8246
1932-6203
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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