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MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes

In contrast to activated CD4(+) T cells and differentiated macrophages, resting CD4(+) T cells and monocytes are non-permissive for HIV-1 replication. The mediators which regulate the resting or quiescent phenotype are often actively involved in the restriction of viral replication and the establish...

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Detalles Bibliográficos
Autores principales: Chiang, Karen, Rice, Andrew P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499811/
https://www.ncbi.nlm.nih.gov/pubmed/23170164
http://dx.doi.org/10.3390/v4091390
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author Chiang, Karen
Rice, Andrew P.
author_facet Chiang, Karen
Rice, Andrew P.
author_sort Chiang, Karen
collection PubMed
description In contrast to activated CD4(+) T cells and differentiated macrophages, resting CD4(+) T cells and monocytes are non-permissive for HIV-1 replication. The mediators which regulate the resting or quiescent phenotype are often actively involved in the restriction of viral replication and the establishment and maintenance of viral latency. Recently, certain microRNAs which are highly expressed in resting cells have been implicated in this capacity, inhibiting the expression of cellular proteins that are also viral co-factors; following activation these microRNAs exhibit decreased expression, while their targets are correspondingly up-regulated, contributing to a favorable milieu for virus replication. Other microRNAs exhibiting a similar expression pattern in resting and activated cells have been shown to directly target the HIV-1 genome. In this review we will discuss the resting state and the causes behind viral restriction in resting cells, with emphasis on the role of microRNAs.
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spelling pubmed-34998112012-11-20 MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes Chiang, Karen Rice, Andrew P. Viruses Review In contrast to activated CD4(+) T cells and differentiated macrophages, resting CD4(+) T cells and monocytes are non-permissive for HIV-1 replication. The mediators which regulate the resting or quiescent phenotype are often actively involved in the restriction of viral replication and the establishment and maintenance of viral latency. Recently, certain microRNAs which are highly expressed in resting cells have been implicated in this capacity, inhibiting the expression of cellular proteins that are also viral co-factors; following activation these microRNAs exhibit decreased expression, while their targets are correspondingly up-regulated, contributing to a favorable milieu for virus replication. Other microRNAs exhibiting a similar expression pattern in resting and activated cells have been shown to directly target the HIV-1 genome. In this review we will discuss the resting state and the causes behind viral restriction in resting cells, with emphasis on the role of microRNAs. MDPI 2012-08-29 /pmc/articles/PMC3499811/ /pubmed/23170164 http://dx.doi.org/10.3390/v4091390 Text en © 2012 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Chiang, Karen
Rice, Andrew P.
MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title_full MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title_fullStr MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title_full_unstemmed MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title_short MicroRNA-Mediated Restriction of HIV-1 in Resting CD4(+) T Cells and Monocytes
title_sort microrna-mediated restriction of hiv-1 in resting cd4(+) t cells and monocytes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499811/
https://www.ncbi.nlm.nih.gov/pubmed/23170164
http://dx.doi.org/10.3390/v4091390
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