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Epigenetic heterogeneity in HIV-1 latency establishment.

Despite prolonged antiretroviral therapy, HIV-1 persists as transcriptionally inactive proviruses. The HIV-1 latency remains a principal obstacle in curing AIDS. It is important to understand mechanisms by which HIV-1 latency is established to make the latent reservoir smaller. We present a molecula... Full description

Journal Title: Scientific reports January 9, 2015, Vol.5, p.7701
Main Author: Matsuda, Yuka
Other Authors: Kobayashi-Ishihara, Mie , Fujikawa, Dai , Ishida, Takaomi , Watanabe, Toshiki , Yamagishi, Makoto
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 2045-2322 ; DOI: 10.1038/srep07701
Link: http://search.proquest.com/docview/1645778394/?pq-origsite=primo
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title: Epigenetic heterogeneity in HIV-1 latency establishment.
format: Article
creator:
  • Matsuda, Yuka
  • Kobayashi-Ishihara, Mie
  • Fujikawa, Dai
  • Ishida, Takaomi
  • Watanabe, Toshiki
  • Yamagishi, Makoto
subjects:
  • Chromatin Immunoprecipitation–Genetics
  • Epigenesis, Genetic–Physiology
  • Genes, Reporter–Metabolism
  • Hek293 Cells–Antagonists & Inhibitors
  • HIV-1–Genetics
  • Histones–Metabolism
  • Humans–Metabolism
  • Jurkat Cells–Genetics
  • Methylation–Genetics
  • Polycomb Repressive Complex 2–Genetics
  • RNA Interference–Genetics
  • RNA, Small Interfering–Genetics
  • Virus Latency–Genetics
  • Histones
  • RNA, Small Interfering
  • Polycomb Repressive Complex 2
ispartof: Scientific reports, January 9, 2015, Vol.5, p.7701
description: Despite prolonged antiretroviral therapy, HIV-1 persists as transcriptionally inactive proviruses. The HIV-1 latency remains a principal obstacle in curing AIDS. It is important to understand mechanisms by which HIV-1 latency is established to make the latent reservoir smaller. We present a molecular characterization of distinct populations at an early phase of infection. We developed an original dual-color reporter virus to monitor LTR kinetics from establishment to maintenance stage. We found that there are two ways of latency establishment i.e., by immediate silencing and slow inactivation from active infection. Histone covalent modifications, particularly polycomb repressive complex 2 (PRC2)-mediated H3K27 trimethylation, appeared to dominate viral transcription at the early phase. PRC2 also contributes to time-dependent LTR dormancy in the chronic phase of the infection. Significant differences in sensitivity against several stimuli were observed between these two distinct populations. These results will expand our understanding of heterogeneous establishment of HIV-1 latency populations.
language: eng
source:
identifier: E-ISSN: 2045-2322 ; DOI: 10.1038/srep07701
fulltext: fulltext
issn:
  • 20452322
  • 2045-2322
url: Link


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titleEpigenetic heterogeneity in HIV-1 latency establishment.
creatorMatsuda, Yuka ; Kobayashi-Ishihara, Mie ; Fujikawa, Dai ; Ishida, Takaomi ; Watanabe, Toshiki ; Yamagishi, Makoto
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ispartofScientific reports, January 9, 2015, Vol.5, p.7701
identifierE-ISSN: 2045-2322 ; DOI: 10.1038/srep07701
subjectChromatin Immunoprecipitation–Genetics ; Epigenesis, Genetic–Physiology ; Genes, Reporter–Metabolism ; Hek293 Cells–Antagonists & Inhibitors ; HIV-1–Genetics ; Histones–Metabolism ; Humans–Metabolism ; Jurkat Cells–Genetics ; Methylation–Genetics ; Polycomb Repressive Complex 2–Genetics ; RNA Interference–Genetics ; RNA, Small Interfering–Genetics ; Virus Latency–Genetics ; Histones ; RNA, Small Interfering ; Polycomb Repressive Complex 2
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descriptionDespite prolonged antiretroviral therapy, HIV-1 persists as transcriptionally inactive proviruses. The HIV-1 latency remains a principal obstacle in curing AIDS. It is important to understand mechanisms by which HIV-1 latency is established to make the latent reservoir smaller. We present a molecular characterization of distinct populations at an early phase of infection. We developed an original dual-color reporter virus to monitor LTR kinetics from establishment to maintenance stage. We found that there are two ways of latency establishment i.e., by immediate silencing and slow inactivation from active infection. Histone covalent modifications, particularly polycomb repressive complex 2 (PRC2)-mediated H3K27 trimethylation, appeared to dominate viral transcription at the early phase. PRC2 also contributes to time-dependent LTR dormancy in the chronic phase of the infection. Significant differences in sensitivity against several stimuli were observed between these two distinct populations. These results will expand our understanding of heterogeneous establishment of HIV-1 latency populations.
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