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Updated: Jan 29, 2026

Amplification of Near Full-length HIV-1 Proviruses for Next-Generation Sequencing
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Amplification of Near Full-length HIV-1 Proviruses for Next-Generation Sequencing

Published on: October 16, 2018

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The Per-1 Short Isoform Inhibits de novo HIV-1 Transcription in Resting CD4+ T-cells

Li Zhao1, Mei Liu1, Jiayue Ouyang1

  • 1Key Laboratory of AIDS Immunology of National Health and Family Planning Commission, Department of Laboratory Medicine, Shenyang, China.

Current HIV Research
|February 19, 2019
PubMed
Abstract

Insights

Per-1 protein restricts human immunodeficiency virus type 1 (HIV-1) replication. Lower Per-1 levels correlate with higher viral loads, suggesting Per-1

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Understanding HIV-1 transcription restriction in resting CD4+ T-cells is crucial for an AIDS cure.
  • While numerous negative factors are known, underlying mechanisms of HIV-1 transcription blockage remain underexplored.

Purpose of the Study:

  • To investigate the molecular mechanisms suppressing de novo HIV-1 transcription in resting CD4+ T-cells.
  • To identify novel regulators of HIV-1 transcription and replication.

Main Methods:

  • Transfected 293T cells with Per-1 expression plasmid, with and without HIV-1 Tat, to assess Per-1's regulatory role.
  • Silenced Per-1 in resting CD4+ T-cells and monocyte-derived macrophages (MDMs) to evaluate its antiviral activity.
  • Analyzed the in vivo correlation between Per-1 expression and viral loads in HIV-1-infected individuals using siRNA.

Main Results:

  • Short isoform Per-1 restricts HIV-1 replication; Tat partially reverses this inhibition.
  • Per-1 silencing upregulates HIV-1 transcription in both resting CD4+ T-cells and MDMs.
  • In vivo, Per-1 expression is inversely correlated with viral loads in rapid progressors.

Conclusions:

  • Per-1 functions as a novel negative regulator of HIV-1 transcription.
  • Per-1's restrictive activity on HIV-1 replication may contribute to viral latency in resting CD4+ T-cells.
Keywords:
HIV-1LTNPsLTRRPsTatresting CD4+ T-cellsviral load.

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