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5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals

We previously described selective hypermethylation of the 5'-long terminal repeat (LTR) of HTLV-1 provirus in vivo and in vitro. This prompted us to analyze CpG methylation of the two LTRs of the HIV provirus in chronically infected cell lines. The results demonstrate selective hypermethylation...

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Autores principales: Ishida, Takaomi, Hamano, Akiko, Koiwa, Tsukasa, Watanabe, Toshiki
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1617119/
https://www.ncbi.nlm.nih.gov/pubmed/17034647
http://dx.doi.org/10.1186/1742-4690-3-69
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author Ishida, Takaomi
Hamano, Akiko
Koiwa, Tsukasa
Watanabe, Toshiki
author_facet Ishida, Takaomi
Hamano, Akiko
Koiwa, Tsukasa
Watanabe, Toshiki
author_sort Ishida, Takaomi
collection PubMed
description We previously described selective hypermethylation of the 5'-long terminal repeat (LTR) of HTLV-1 provirus in vivo and in vitro. This prompted us to analyze CpG methylation of the two LTRs of the HIV provirus in chronically infected cell lines. The results demonstrate selective hypermethylation of the 5' LTR of the HIV provirus in ACH-2 cells. Moreover, induction of viral gene expression by TNF-α resulted in demethylation of the 5'-LTR. These results suggest that selective epigenetic modification of the 5'LTR of the HIV-1 provirus may be an important mechanism by which proviral activity is suppressed.
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spelling pubmed-16171192006-10-19 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals Ishida, Takaomi Hamano, Akiko Koiwa, Tsukasa Watanabe, Toshiki Retrovirology Short Report We previously described selective hypermethylation of the 5'-long terminal repeat (LTR) of HTLV-1 provirus in vivo and in vitro. This prompted us to analyze CpG methylation of the two LTRs of the HIV provirus in chronically infected cell lines. The results demonstrate selective hypermethylation of the 5' LTR of the HIV provirus in ACH-2 cells. Moreover, induction of viral gene expression by TNF-α resulted in demethylation of the 5'-LTR. These results suggest that selective epigenetic modification of the 5'LTR of the HIV-1 provirus may be an important mechanism by which proviral activity is suppressed. BioMed Central 2006-10-12 /pmc/articles/PMC1617119/ /pubmed/17034647 http://dx.doi.org/10.1186/1742-4690-3-69 Text en Copyright © 2006 Ishida et al; 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 Short Report
Ishida, Takaomi
Hamano, Akiko
Koiwa, Tsukasa
Watanabe, Toshiki
5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title_full 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title_fullStr 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title_full_unstemmed 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title_short 5' long terminal repeat (LTR)-selective methylation of latently infected HIV-1 provirus that is demethylated by reactivation signals
title_sort 5' long terminal repeat (ltr)-selective methylation of latently infected hiv-1 provirus that is demethylated by reactivation signals
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1617119/
https://www.ncbi.nlm.nih.gov/pubmed/17034647
http://dx.doi.org/10.1186/1742-4690-3-69
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