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Related Experiment Videos

NFAT1 enhances HIV-1 gene expression in primary human CD4 T cells.

R Q Cron1, S R Bartz, A Clausell

  • 1Division of Immunology and Transplantation Biology, Stanford University Medical Center, Palo Alto, California 94304-5208, USA.

Clinical Immunology (Orlando, Fla.)
|February 29, 2000
PubMed
Summary

Cyclosporin A (CsA) inhibits Nuclear Factor of Activated T cells (NFAT). This study shows NFAT directly enhances human immunodeficiency virus type 1 (HIV-1) transcription, suggesting NFAT as a potential therapeutic target.

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Cyclosporin A (CsA) inhibits NFAT, a key factor in T cell activation.
  • Reduced HIV-1 viral load observed in CsA-treated patients suggests NFAT's role in HIV-1 transcription.

Purpose of the Study:

  • To investigate the direct role of NFAT in enhancing HIV-1 transcription.
  • To explore NFAT as a potential therapeutic target for controlling HIV-1 gene expression.

Main Methods:

  • In vitro footprinting and gel shift analysis to identify NFAT binding sites on the HIV-1 LTR.
  • Reporter gene assays in CD4 T cells to assess HIV-1 LTR promoter activity.
  • Transfection of CD4 T cells with HIV-1 provirus to measure p24 protein expression.

Main Results:

Related Experiment Videos

  • NFAT1 specifically binds to NFkappaB sites within the HIV-1 LTR.
  • NFAT1 expression enhances HIV-1 LTR-driven gene expression.
  • CsA, FK506, and dominant-negative NFAT1 inhibit HIV-1 LTR promoter activity.

Conclusions:

  • NFAT plays a direct role in enhancing HIV-1 LTR-directed gene expression.
  • NFAT is a potential target for therapeutic strategies aimed at preventing HIV-1 replication.