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Immune Cells Release MicroRNA-155 Enriched Extracellular Vesicles That Promote HIV-1 Infection.

Julien Boucher1, Alyssa Rousseau1, Catherine Boucher1

  • 1Axe de Recherche Maladies Infectieuses et Immunitaires, Centre de Recherche du CHU de Québec-Université Laval, Québec, QC G1V 4G2, Canada.

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|February 11, 2023
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Summary

Activation of immune cells in people living with HIV (PLWH) releases extracellular vesicles (EVs) containing microRNA-155. These miR-155-rich EVs promote HIV-1 replication, potentially worsening infection.

Keywords:
HIV-1TRL7/8calprotectinextracellular vesiclesimmune activationinflammationmiR-155micro-RNApathogenesis

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • HIV-1 infection causes immune dysregulation.
  • Extracellular vesicles (EVs) enriched with microRNA-155 (miR-155) correlate with immune activation and viral rebound in people living with HIV (PLWH).
  • Peripheral blood mononuclear cells (PBMCs) are key immune cells affected by HIV-1.

Purpose of the Study:

  • To investigate if activated PBMCs increase miR-155 expression and produce miR-155-rich EVs.
  • To determine if these miR-155-rich EVs exacerbate HIV-1 replication in PBMCs.
  • To explore the role of autocrine loops in HIV-1 pathogenesis.

Main Methods:

  • PBMCs were incubated with HIV-1, a TLR-7/8 agonist, or TNF.
  • Extracellular vesicles (EVs) were isolated from cell culture supernatants via differential centrifugation.
  • MicroRNA-155 (miR-155) levels in cells and EVs were quantified using RT-qPCR.
  • The impact of miR-155-rich EVs on HIV-1 replication was assessed by quantifying viral RNA and DNA.

Main Results:

  • HIV-1, TLR-7/8 agonist, and TNF each stimulated PBMCs to release EVs enriched with miR-155.
  • Exposure to these miR-155-rich EVs significantly increased HIV-1 replication in incubated PBMCs.
  • This suggests miR-155-rich EVs promote viral replication in an in vitro model.

Conclusions:

  • HIV-1 infection and inflammation stimulate PBMCs to produce miR-155-rich EVs.
  • These EVs enhance HIV-1 replication, indicating a potential mechanism for disease progression.
  • Autocrine loops involving miR-155-rich EVs may influence the course of HIV-1 infection.