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SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells

Resting CD4(+) T-cells are critical for establishing HIV-1 reservoirs. It has been known for over two decades that resting CD4(+) T-cells are refractory to HIV-1 infection, but the underlying mechanisms are not fully understood. Compared with activated CD4(+) T-cells that support HIV-1 infection, re...

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Detalles Bibliográficos
Autor principal: Wu, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492151/
https://www.ncbi.nlm.nih.gov/pubmed/23092163
http://dx.doi.org/10.1186/1742-4690-9-88
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author Wu, Li
author_facet Wu, Li
author_sort Wu, Li
collection PubMed
description Resting CD4(+) T-cells are critical for establishing HIV-1 reservoirs. It has been known for over two decades that resting CD4(+) T-cells are refractory to HIV-1 infection, but the underlying mechanisms are not fully understood. Compared with activated CD4(+) T-cells that support HIV-1 infection, resting CD4(+) T-cells have lower levels of dNTPs, which limit HIV-1 reverse transcription. The dNTPase SAMHD1 has been identified as an HIV-1 restriction factor in non-cycling myeloid cells. Two recent studies revealed that SAMHD1 restricts HIV-1 infection in resting CD4(+) T-cells, suggesting a common mechanism of HIV-1 restriction in non-cycling cells that may contribute to viral immunopathogenesis.
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spelling pubmed-34921512012-11-08 SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells Wu, Li Retrovirology Viewpoints Resting CD4(+) T-cells are critical for establishing HIV-1 reservoirs. It has been known for over two decades that resting CD4(+) T-cells are refractory to HIV-1 infection, but the underlying mechanisms are not fully understood. Compared with activated CD4(+) T-cells that support HIV-1 infection, resting CD4(+) T-cells have lower levels of dNTPs, which limit HIV-1 reverse transcription. The dNTPase SAMHD1 has been identified as an HIV-1 restriction factor in non-cycling myeloid cells. Two recent studies revealed that SAMHD1 restricts HIV-1 infection in resting CD4(+) T-cells, suggesting a common mechanism of HIV-1 restriction in non-cycling cells that may contribute to viral immunopathogenesis. BioMed Central 2012-10-23 /pmc/articles/PMC3492151/ /pubmed/23092163 http://dx.doi.org/10.1186/1742-4690-9-88 Text en Copyright ©2012 Wu; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Viewpoints
Wu, Li
SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title_full SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title_fullStr SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title_full_unstemmed SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title_short SAMHD1: a new contributor to HIV-1 restriction in resting CD4(+) T-cells
title_sort samhd1: a new contributor to hiv-1 restriction in resting cd4(+) t-cells
topic Viewpoints
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492151/
https://www.ncbi.nlm.nih.gov/pubmed/23092163
http://dx.doi.org/10.1186/1742-4690-9-88
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