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Molecular circuitry regulating herpes simplex virus type 1 latency in neurons
1The Pennsylvania State University College of Medicine, Department of Microbiology and Immunology, Hershey 17033, USA.
Journal of Neurovirology
|April 29, 2000
Summary
Herpes simplex virus type 1 (HSV-1) establishes latency in neurons. The major latency-associated transcripts (LATs) play a crucial role in maintaining HSV-1 latency and facilitating viral reactivation.
Area of Science:
- Virology
- Neuroscience
- Molecular Biology
Background:
- Herpes simplex virus type 1 (HSV-1) establishes lifelong latency in sensory neurons.
- Latency is characterized by minimal viral gene expression, with high expression of latency-associated transcripts (LATs).
Purpose of the Study:
- To review the structure, expression, and function of HSV-1 LATs.
- To explore mechanisms linking LATs to latency establishment and viral reactivation.
Main Methods:
- Literature review of studies on HSV-1 latency and LATs.
- Analysis of experimental evidence on LATs' role in latency and reactivation.
- Proposal of a model for LAT locus involvement in HSV-1 latency.
Main Results:
- LATs are highly expressed during HSV-1 latency.
- LAT transcription may facilitate latency establishment and increase reactivation frequency.
- Host factors interact with viral gene expression impacting latency.
Conclusions:
- The HSV-1 LAT locus is central to the biology of latency.
- Understanding LATs' function and regulation is key to controlling HSV-1 reactivation.