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Herpes simplex virus latency in the nervous system--a new model
1Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
Neuropathology and Applied Neurobiology
|December 1, 1991
Summary
Herpes simplex virus (HSV) latency and reactivation in neurons do not cause cell death. Latency is established in non-replicating neurons, and reactivation involves peripheral viral replication or non-damaging neuronal replication, preserving neuronal reservoirs.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Herpes simplex virus (HSV) infection causes cell destruction in vitro.
- In vivo, latent HSV infection occurs in peripheral sensory ganglia (PSG) neurons.
- Previous understanding suggested lytic replication precedes latency.
Purpose of the Study:
- To propose a model for HSV-1 latency and reactivation that does not involve neuronal cell loss.
- To investigate the role of the viral transactivating protein Vmw65 in latency establishment.
- To explain the persistence of HSV in neurons throughout the host's life.
Main Methods:
- Review of experimental data and human observations.
- Hypothesis formulation based on existing knowledge.
- Theoretical modeling of HSV latency and reactivation.
Main Results:
- Latency is established in neurons where HSV does not replicate.
- Tissue levels of Vmw65 influence latency establishment.
- Reactivation does not necessitate neuronal destruction, occurring via peripheral replication or non-damaging neuronal replication.
Conclusions:
- HSV latency and reactivation do not involve neuronal cell loss.
- Neurons serve as permanent reservoirs for latent HSV.
- The proposed model explains the long-term persistence of HSV without damaging host neurons.