Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Combination treatment with synthetic gRNA/Cas12a and gRNA/Cas9 ribonucleoproteins disrupts HIV replication and expression.

iScience·2026
Same author

Extracellular Vesicles: A Comprehensive Review of Their Origins, Functions, and Therapeutic Potential.

Biomedicines·2026
Same author

Suppression of HBV replication and expression by CRISPR/Cas9 ribonucleoproteins.

Antiviral research·2025
Same author

Inhibition of protein kinase R suppresses HIV replication and integration in CD4 T cells.

Journal of virus eradication·2025
Same author

IRF4 Mediates Immune Evasion to Facilitate EBV Transformation.

Viruses·2025
Same author

An Exploratory Pharmacogenetic Pilot Study of Two Reverse Transcriptase Inhibitors, Tenofovir Alafenamide Fumarate and Tenofovir Disoproxil Fumarate.

Drugs in R&D·2025

Related Experiment Video

Updated: May 16, 2025

New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
09:27

New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals

Published on: May 30, 2013

11.1K

miR-23a-mediated TRF2 repression in CD4 T cells from PLWH.

Lam N T Nguyen1, Juan Zhao1, Jaeden S Pyburn1

  • 1Center of Excellence in Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States; Department of Internal Medicine, Division of Infectious, Inflammatory and Immunologic Diseases, Quillen College of Medicine, ETSU, Johnson City, TN, United States.

Molecular Immunology
|April 20, 2025
PubMed
Summary

MicroRNA-23a (miR-23a) is elevated in HIV patients, suppressing TRF2 protein and accelerating CD4 T cell aging. Targeting miR-23a may restore T cell function and telomere integrity in people living with HIV.

Keywords:
CD4 T cell agingHIVTRF2miR-23a

More Related Videos

Isolation, Transfection, and Culture of Primary Human Monocytes
09:13

Isolation, Transfection, and Culture of Primary Human Monocytes

Published on: December 16, 2019

13.2K
Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
08:11

Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.

Published on: September 1, 2015

8.7K

Related Experiment Videos

Last Updated: May 16, 2025

New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
09:27

New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals

Published on: May 30, 2013

11.1K
Isolation, Transfection, and Culture of Primary Human Monocytes
09:13

Isolation, Transfection, and Culture of Primary Human Monocytes

Published on: December 16, 2019

13.2K
Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
08:11

Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.

Published on: September 1, 2015

8.7K

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • CD4 T cells in people living with HIV (PLWH) on antiretroviral therapy (ART) display inflammaging, characterized by inflammation, immune activation, exhaustion, senescence, and apoptosis.
  • Previous studies showed that telomeric repeat factor 2 (TRF2) inhibition accelerates telomere erosion and CD4 T cell aging in PLWH.

Purpose of the Study:

  • To investigate the microRNA (miRNA)-mediated mechanism inhibiting TRF2 protein in CD4 T cells of PLWH.
  • To explore the potential of targeting miR-23a to restore CD4 T cell function in PLWH.

Main Methods:

  • Quantification of miR-23a and TRF2 protein in CD4 T cells from PLWH and healthy subjects (HS).
  • Bioinformatics analysis to identify potential miRNA targets of TRF2.
  • Luciferase reporter assays to confirm miR-23a's suppression of TRF2 translation.
  • T cell receptor (TCR) activation experiments.
  • miR-23a mimic and knockdown studies in CD4 T cells.

Main Results:

  • miR-23a was significantly increased, and TRF2 protein repressed, in CD4 T cells from PLWH compared to HS.
  • Bioinformatics predicted and luciferase assays confirmed TRF2 3'UTR as a target of miR-23a, suppressing TRF2 translation.
  • TCR activation increased miR-23a and decreased TRF2 expression in CD4 T cells from both PLWH and HS.
  • Overexpression of miR-23a in HS CD4 T cells mimicked the PLWH phenotype (decreased TRF2, increased apoptosis).
  • miR-23a knockdown in PLWH CD4 T cells increased TRF2 protein levels.

Conclusions:

  • miR-23a negatively regulates TRF2 protein expression in CD4 T cells.
  • Elevated miR-23a contributes to TRF2 repression and CD4 T cell aging in PLWH.
  • Targeting miR-23a presents a potential therapeutic strategy to increase TRF2, protect telomere integrity, and restore CD4 T cell function in PLWH.