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APOBEC3G & HTLV-1: Inhibition without deamination

APOBEC3G is a cellular cytidine deaminase that was recently identified as the Vif-sensitive antiviral host factor responsible for the restriction of vif-defective HIV-1 in primary human cells and certain non-permissive T cell lines. Inhibition of HIV-1 replication is thought to be the result of APOB...

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Detalles Bibliográficos
Autor principal: Strebel, Klaus
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156953/
https://www.ncbi.nlm.nih.gov/pubmed/15921532
http://dx.doi.org/10.1186/1742-4690-2-37
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author Strebel, Klaus
author_facet Strebel, Klaus
author_sort Strebel, Klaus
collection PubMed
description APOBEC3G is a cellular cytidine deaminase that was recently identified as the Vif-sensitive antiviral host factor responsible for the restriction of vif-defective HIV-1 in primary human cells and certain non-permissive T cell lines. Inhibition of HIV-1 replication is thought to be the result of APOBEC3G-induced hypermutation of the viral genome that occurs early during reverse transcription. Against this backdrop is a new report from the Uchiyama laboratory that proposes deaminase-independent restriction of HTLV-1 by APOBEC3G (Sasada et al. Retrovirology 2005, 2:32). These findings combined with recent reports of deaminase-independent inhibition of Hepatitis B virus as well as HIV-1 suggest that cytidine deaminase activity and antiviral activity may be separable functional properties of APOBEC3G.
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spelling pubmed-11569532005-06-22 APOBEC3G & HTLV-1: Inhibition without deamination Strebel, Klaus Retrovirology Commentary APOBEC3G is a cellular cytidine deaminase that was recently identified as the Vif-sensitive antiviral host factor responsible for the restriction of vif-defective HIV-1 in primary human cells and certain non-permissive T cell lines. Inhibition of HIV-1 replication is thought to be the result of APOBEC3G-induced hypermutation of the viral genome that occurs early during reverse transcription. Against this backdrop is a new report from the Uchiyama laboratory that proposes deaminase-independent restriction of HTLV-1 by APOBEC3G (Sasada et al. Retrovirology 2005, 2:32). These findings combined with recent reports of deaminase-independent inhibition of Hepatitis B virus as well as HIV-1 suggest that cytidine deaminase activity and antiviral activity may be separable functional properties of APOBEC3G. BioMed Central 2005-05-29 /pmc/articles/PMC1156953/ /pubmed/15921532 http://dx.doi.org/10.1186/1742-4690-2-37 Text en Copyright © 2005 Strebel; 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 Commentary
Strebel, Klaus
APOBEC3G & HTLV-1: Inhibition without deamination
title APOBEC3G & HTLV-1: Inhibition without deamination
title_full APOBEC3G & HTLV-1: Inhibition without deamination
title_fullStr APOBEC3G & HTLV-1: Inhibition without deamination
title_full_unstemmed APOBEC3G & HTLV-1: Inhibition without deamination
title_short APOBEC3G & HTLV-1: Inhibition without deamination
title_sort apobec3g & htlv-1: inhibition without deamination
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156953/
https://www.ncbi.nlm.nih.gov/pubmed/15921532
http://dx.doi.org/10.1186/1742-4690-2-37
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