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Related Experiment Videos

STAT1 binds to the herpes simplex virus type 1 latency-associated transcript promoter.

John D Kriesel1, Brandt B Jones, Kimberly M Dahms

  • 1Department of Opthalomology, John A. Moran Eye Center, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA. jkriesel@med.utah.edu

Journal of Neurovirology
|February 26, 2004
PubMed
Summary

Herpes Simplex Virus type 1 (HSV-1) reactivation may be regulated by STAT1 binding to the LAT promoter. This interaction, involving signal transducers and activators of transcription (STATs), influences viral gene expression and latency.

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Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Herpes Simplex Virus type 1 (HSV-1) reactivation is a complex process.
  • The latency-associated transcript (LAT) gene plays a role in HSV-1 reactivation.
  • Environmental stimuli and cytokines are implicated in viral reactivation through intracellular signaling cascades.

Purpose of the Study:

  • To investigate the role of signal transducers and activators of transcription (STATs) in regulating HSV-1 gene expression and reactivation.
  • To determine if STAT transcription factors bind to the 3' region of the HSV-1 LAT promoter.
  • To explore the mechanism by which environmental stimuli might induce viral reactivation.

Main Methods:

  • Electrophoretic mobility shift assay (EMSA) was used to analyze the binding of nuclear extracts to HSV-1 LAT promoter sequences.

Related Experiment Videos

  • Nuclear extracts from mouse trigeminal ganglia were incubated with overlapping oligonucleotide sequences (L1, L2, L3) of the LAT promoter's 3' region.
  • Antibodies against STAT1, STAT3, and STAT5a were used to identify specific STAT protein binding.

    • Main Results:

    • Nuclear extracts specifically bound to LAT promoter sequences L1 and L3, which contain predicted STAT binding sites.
    • STAT1 antibodies caused a supershift in binding to oligo L3, indicating STAT1 interaction.
    • Binding to L3 was reduced by competition with STAT1 consensus sequences, further supporting STAT1 involvement.

    Conclusions:

    • STAT1, potentially as part of a complex, binds to the HSV-1 LAT promoter near the TATA box.
    • This binding supports the hypothesis that STAT1 mediates the effects of interferons on HSV-1 LAT expression.
    • Further research is needed to confirm STAT1's requirement for LAT expression in vivo during viral reactivation.