Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript
G C Perng1, C Jones, J Ciacci-Zanella
1Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns & Allen Research Institute, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.
Science (New York, N.Y.)
|February 26, 2000
Summary
Herpes simplex virus (HSV) latency involves a gene called the latency-associated transcript (LAT). This LAT gene is crucial for HSV reactivation and promotes neuronal survival by preventing apoptosis.
Area of Science:
- Virology
- Neuroscience
- Molecular Biology
Background:
- Latent infections with periodic reactivation are common after acute viral infections.
- The latency-associated transcript (LAT) gene is essential for wild-type herpes simplex virus (HSV) reactivation.
- The precise mechanisms by which LAT influences latency and reactivation are not fully understood.
Discussion:
- Extensive apoptosis was observed in rabbit trigeminal ganglia infected with LAT-negative (LAT(-)) HSV.
- In contrast, LAT-positive (LAT(+)) HSV infections did not result in significant apoptosis.
- A plasmid expressing LAT demonstrated the ability to inhibit apoptosis in cultured cells.
Key Insights:
- The LAT gene plays a critical role in promoting neuronal survival during HSV-1 infection.
- LAT actively reduces apoptosis, a key factor in maintaining viral latency.
- This finding clarifies a crucial aspect of the HSV life cycle and pathogenesis.
Outlook:
- Further research into LAT's anti-apoptotic mechanisms could reveal novel therapeutic targets.
- Understanding LAT's role may lead to strategies for preventing HSV reactivation.
- Investigating LAT's function in other neurological contexts could broaden its implications.
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