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Related Experiment Videos

Herpes simplex virus latency-associated transcript is a stable intron.

M J Farrell1, A T Dobson, L T Feldman

  • 1Molecular Biology Institute, University of California, Los Angeles 90024.

Proceedings of the National Academy of Sciences of the United States of America
|February 1, 1991
PubMed
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The herpes simplex virus type 1 latency-associated transcript (LAT) is a stable intron that inhibits viral reactivation. This finding offers new insights into controlling herpes simplex virus type 1 latency.

Area of Science:

  • Virology
  • Molecular Biology
  • Gene Regulation

Background:

  • Herpes simplex virus type 1 (HSV-1) establishes latency in sensory ganglia.
  • The latency-associated transcript (LAT) is the major viral transcript during HSV-1 latency.
  • LAT's role in viral reactivation is not fully understood, though it's complementary to ICP0, a key viral transactivator.

Purpose of the Study:

  • To elucidate the nature and function of the latency-associated transcript (LAT) in HSV-1 latency.
  • To investigate the mechanism by which LAT might regulate viral reactivation.
  • To determine LAT's interaction with infected-cell polypeptide 0 (ICP0).

Main Methods:

  • In situ hybridization to detect LAT in infected ganglia.
  • Analysis of LAT's complementarity to infected-cell polypeptide 0 (ICP0).

Related Experiment Videos

  • Transient transfection assays to assess LAT's effect on gene expression and ICP0-mediated transactivation.

    • Main Results:

    • LAT is identified as a uniquely stable intron, not a polyadenylylated mRNA.
    • The LAT promoter is located 688 bases upstream of its 5' end.
    • LAT significantly inhibits gene expression transactivation by ICP0 in transfection assays.

    Conclusions:

    • The latency-associated transcript (LAT) is a stable intron that actively suppresses viral gene expression.
    • LAT's inhibitory effect on ICP0-mediated transactivation suggests a novel mechanism for maintaining HSV-1 latency.
    • These findings provide a molecular basis for LAT's role in preventing viral reactivation.