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Related Experiment Video

Updated: Aug 16, 2025

Humanized NOD/SCID/IL2r&#947;null (hu-NSG) Mouse Model for HIV Replication and Latency Studies
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Transcriptomic Signatures of Human Immunodeficiency Virus Post-Treatment Control.

Adam Wedrychowski1,2, Holly Anne Martin1,2, Yijia Li3

  • 1Department of Medicine, University of California, San Francisco, California, USA.

Journal of Virology
|December 21, 2022
PubMed
Summary
This summary is machine-generated.

Rare individuals called posttreatment controllers (PTCs) can control HIV after stopping therapy. This study reveals PTCs limit multiply-spliced HIV RNA early and show distinct cellular gene expression, offering insights into functional HIV cure strategies.

Keywords:
ARTHIV DNAHIV posttreatment controllersRNA splicinganalytic treatment interruptioncell-mediated immune responsehuman immunodeficiency virusnoncontrollerssplicingtranscriptiontranscriptional completiontranscriptional profiletreatment interruptionviremic suppression

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Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Posttreatment controllers (PTCs) rarely control HIV after antiretroviral therapy interruption (ATI).
  • Mechanisms underlying this posttreatment control remain unclear.
  • Understanding these mechanisms is crucial for developing strategies towards a functional HIV cure.

Purpose of the Study:

  • To investigate the molecular mechanisms of posttreatment control.
  • To compare HIV and cellular gene expression in PTCs and noncontrollers (NCs) before and after ATI.
  • To identify correlates or mechanisms of posttreatment control.

Main Methods:

  • Quantification of HIV RNA transcripts using reverse transcription droplet digital PCR (RT-ddPCR).
  • Analysis of cellular transcriptomes via RNA-sequencing (RNA-seq).
  • Comparison of gene expression profiles in blood cells from PTCs and NCs at multiple time points.

Main Results:

  • PTCs showed no increase in multiply-spliced HIV RNA after ATI, unlike NCs.
  • PTCs exhibited a delayed reduction in completed HIV transcripts post-ATI.
  • Differential expression of cytokine, inflammation, HIV transcription, and cell death pathways was observed between PTCs and NCs.

Conclusions:

  • Posttreatment control is associated with early limitation of spliced HIV RNA and delayed reversal of completed HIV transcripts.
  • Distinct cellular gene expression pathways, including IL-7, p53, and TNF, differentiate PTCs from NCs.
  • These molecular differences offer insights into potential therapeutic targets for achieving a functional HIV cure.