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APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection

BACKGROUND: CD4+ T lymphocytes are the primary targets of HIV1 but cannot be infected when fully quiescent, due to a post-entry block preventing the completion of reverse transcription. Chiu et al. recently proposed that this restriction reflects the action of APOBEC3G (A3G). They further suggested...

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Autores principales: Santoni de Sio, Francesca R., Trono, Didier
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719058/
https://www.ncbi.nlm.nih.gov/pubmed/19668336
http://dx.doi.org/10.1371/journal.pone.0006571
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author Santoni de Sio, Francesca R.
Trono, Didier
author_facet Santoni de Sio, Francesca R.
Trono, Didier
author_sort Santoni de Sio, Francesca R.
collection PubMed
description BACKGROUND: CD4+ T lymphocytes are the primary targets of HIV1 but cannot be infected when fully quiescent, due to a post-entry block preventing the completion of reverse transcription. Chiu et al. recently proposed that this restriction reflects the action of APOBEC3G (A3G). They further suggested that T cell activation abrogates the A3G-mediated block by directing this protein to a high molecular mass complex. METHODOLOGY/PRINCIPAL FINDINGS: In the present work, we sought to explore further this model. However, we found that effective suppression of A3G by combined RNA interference and expression of HIV1 Vif does not relieve the restrictive phenotype of post-activation resting T cells. We also failed to find a correlation between HIV resistance and the presence of A3G in a low molecular complex in primary T cells. CONCLUSIONS/SIGNIFICANCE: We conclude that A3G is unlikely to play a role in the HIV restrictive phenotype of quiescent T lymphocytes.
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spelling pubmed-27190582009-08-10 APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection Santoni de Sio, Francesca R. Trono, Didier PLoS One Research Article BACKGROUND: CD4+ T lymphocytes are the primary targets of HIV1 but cannot be infected when fully quiescent, due to a post-entry block preventing the completion of reverse transcription. Chiu et al. recently proposed that this restriction reflects the action of APOBEC3G (A3G). They further suggested that T cell activation abrogates the A3G-mediated block by directing this protein to a high molecular mass complex. METHODOLOGY/PRINCIPAL FINDINGS: In the present work, we sought to explore further this model. However, we found that effective suppression of A3G by combined RNA interference and expression of HIV1 Vif does not relieve the restrictive phenotype of post-activation resting T cells. We also failed to find a correlation between HIV resistance and the presence of A3G in a low molecular complex in primary T cells. CONCLUSIONS/SIGNIFICANCE: We conclude that A3G is unlikely to play a role in the HIV restrictive phenotype of quiescent T lymphocytes. Public Library of Science 2009-08-10 /pmc/articles/PMC2719058/ /pubmed/19668336 http://dx.doi.org/10.1371/journal.pone.0006571 Text en Santoni de Sio, Trono. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Santoni de Sio, Francesca R.
Trono, Didier
APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title_full APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title_fullStr APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title_full_unstemmed APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title_short APOBEC3G-Depleted Resting CD4(+) T Cells Remain Refractory to HIV1 Infection
title_sort apobec3g-depleted resting cd4(+) t cells remain refractory to hiv1 infection
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719058/
https://www.ncbi.nlm.nih.gov/pubmed/19668336
http://dx.doi.org/10.1371/journal.pone.0006571
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