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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing
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Published on: January 22, 2019

Three rules for HIV latency: location, location, and location.

Melanie Ott1, Eric Verdin

  • 1Gladstone Institutes, University of California, San Francisco, 1650 Owens Street, San Francisco, CA 94941, USA. mott@gladstone.ucsf.edu

Cell Host & Microbe
|June 18, 2013
PubMed
Summary

HIV latency, a hurdle to eradication, is established when proviral DNA is positioned near promyelocytic leukemia (PML) nuclear bodies. This reversible process recruits the G9a enzyme to the viral promoter.

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Area of Science:

  • Molecular Biology
  • Virology
  • Epigenetics

Background:

  • Human immunodeficiency virus (HIV) latency poses a significant challenge to eradicating the virus from infected individuals.
  • Understanding the mechanisms establishing and maintaining HIV latency is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the role of promyelocytic leukemia (PML) nuclear bodies in the establishment of HIV latency.
  • To identify the molecular players involved in the spatial positioning of proviral chromatin relative to PML nuclear bodies.

Main Methods:

  • Chromatin immunoprecipitation (ChIP) assays to analyze the localization of proviral DNA and associated proteins.
  • Immunofluorescence microscopy to visualize the proximity of HIV provirus to PML nuclear bodies.
  • Biochemical assays to assess the recruitment of methyltransferase enzymes like G9a.

Main Results:

  • HIV latency is established through the spatial positioning of proviral chromatin in close proximity to PML nuclear bodies.
  • This proximity is a reversible process, suggesting potential for therapeutic intervention.
  • The methyltransferase enzyme G9a is recruited to the latent viral promoter in association with PML bodies.

Conclusions:

  • PML nuclear bodies play a critical role in establishing HIV latency by organizing proviral chromatin.
  • The recruitment of G9a to the latent viral promoter, mediated by PML bodies, is a key epigenetic event in silencing HIV.
  • Targeting the interaction between PML bodies and proviral chromatin may offer a novel strategy for HIV reactivation and eradication.