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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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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2005
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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. |
format | Text |
id | pubmed-1156953 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT strebelklaus apobec3ghtlv1inhibitionwithoutdeamination |