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Related Experiment Videos

HSV LAT and neuronal survival.

David C Bloom1

  • 1Department of Molecular Genetics & Microbiology, University of Florida College of Medicine, Gainesville, Florida 32610-0266, USA. dbloom@ufl.edu

International Reviews of Immunology
|December 24, 2003
PubMed
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The Herpes Simplex Virus (HSV) latency-associated transcript (LAT) is crucial for viral reactivation and persistence. LAT enhances HSV reactivation and inhibits neuronal cell death, contributing to lifelong infection.

Area of Science:

  • Virology
  • Neuroscience
  • Molecular Biology

Background:

  • Herpes Simplex Virus (HSV) establishes lifelong latent infections in sensory neurons.
  • HSV latency involves tightly regulated viral functions to prevent neuronal damage and uncontrolled viral spread.
  • The HSV latency-associated transcript (LAT) is a key viral element expressed during latency.

Purpose of the Study:

  • To investigate the role of the HSV latency-associated transcript (LAT) in the viral latency-reactivation cycle.
  • To understand how LAT influences viral reactivation, latency establishment, and virulence.
  • To explore LAT's function in inhibiting neuronal apoptosis.

Main Methods:

  • Analysis of LAT mutations to assess their impact on viral replication, latency, and reactivation.

Related Experiment Videos

  • Investigating the effect of LAT on neuronal cell death pathways, specifically caspase-8 and caspase-9.
  • Evaluating LAT's contribution to HSV persistence and spread within the host.
  • Main Results:

    • Mutational analyses show LAT is nonessential for viral replication but significantly enhances reactivation.
    • Specific LAT mutations reduce latency establishment and increase viral virulence.
    • LAT inhibits apoptosis by blocking caspase-8 and caspase-9 pathways, augmenting latency and reactivation.

    Conclusions:

    • The HSV LAT plays a critical role in regulating the latency-reactivation cycle.
    • LAT's ability to enhance reactivation and inhibit apoptosis contributes to HSV's long-term persistence and neuronal survival.