Related Experiment Videos
The continuing problem of herpes simplex virus persistence
Acta Virologica
|September 1, 1983
Summary
Herpes simplex virus (HSV) establishes lifelong latent infections in nerve ganglia. Reactivation causes recurrent disease, but ganglia are typically non-infectious during latency.
Area of Science:
- Virology
- Neuroscience
- Infectious Diseases
Background:
- Herpes simplex virus (HSV) pathogenesis research shifted from acute to latent infections in the 1970s.
- HSV persistence remains a significant challenge in both clinical and theoretical contexts.
- Understanding HSV latency is crucial for managing recurrent infections.
Purpose of the Study:
- To summarize the current understanding of herpes simplex virus (HSV) latency and persistence.
- To elucidate the mechanisms of HSV neural spread and lifelong residency.
- To describe the intermittent reactivation patterns of HSV.
Main Methods:
- Review of existing literature on HSV pathogenesis and latency.
- Analysis of studies investigating HSV neural tropism.
- Examination of evidence for non-productive viral persistence in ganglia.
Main Results:
- HSV disseminates along neuronal pathways, both intra- and extra-axonally.
- The virus establishes a non-productive, lifelong latent state within sensory or autonomic ganglia.
- Intermittent viral reactivation leads to peripheral shedding or recurrent clinical manifestations.
Conclusions:
- HSV latency involves minimal viral transcription and translation within neurons.
- Despite viral DNA presence, ganglia are largely non-infectious during latency.
- HSV persistence highlights the complex interplay between the virus and the host nervous system.