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Neuronal control of herpes simplex virus latency
R B Tenser1, W A Edris, K A Hay
1Department of Medicine (Neurology), Penn State University College of Medicine, Hershey 17033.
Virology
|August 1, 1993
Summary
Sciatic neurectomy significantly reduced herpes simplex virus (HSV) latency-associated transcript (LAT) and HSV DNA in mouse dorsal root ganglia. This suggests neuronal control mechanisms influence HSV latency.
Area of Science:
- Neurovirology
- Molecular Neuroscience
Background:
- Herpes simplex virus (HSV) establishes lifelong latent infections in sensory neurons.
- During latency, viral transcription is restricted, primarily to latency-associated transcript (LAT).
- The regulation of HSV latency by neuronal function remains incompletely understood.
Purpose of the Study:
- To investigate the impact of altered nervous system function on HSV latent infection.
- To examine the effect of sciatic neurectomy on HSV LAT and DNA levels in dorsal root ganglia (DRG).
Main Methods:
- Latent HSV infection was established in mouse lumbar DRG via footpad inoculation.
- Sciatic neurectomy was performed to alter neuronal function during latency.
- HSV LAT expression was quantified using in situ and Northern blot hybridization.
- HSV DNA levels were assessed by polymerase chain reaction (PCR).
Main Results:
- Neurectomy led to a marked decrease in LAT-positive neurons and overall ganglion LAT levels.
- This reduction in LAT was observed in both thymidine kinase-positive (TK+) and TK- HSV infections.
- A significant decrease in HSV DNA was also detected in DRG after neurectomy.
Conclusions:
- Neurectomy-induced changes in neuronal transcription likely reduce HSV LAT expression.
- Decreased LAT expression may contribute to reduced HSV DNA and overall latency.
- These findings highlight the critical role of neuronal control in HSV latent infection pathogenesis.