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Neuronal dysfunction and death in rabies virus infection
1Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens, GA 30602, USA. zhanfu@vet.uga.edu
Journal of Neurovirology
|April 5, 2005
Summary
Rabies virus causes severe disease through neuronal dysfunction, not just mild morphologic changes. Apoptosis may contribute to neuronal death, but its role in natural rabies requires further study.
Area of Science:
- Neuroscience
- Virology
- Pathology
Background:
- Morphologic changes in natural rabies are typically mild.
- Severe rabies disease and fatality are linked to neuronal dysfunction in infected neurons.
- The exact mechanisms of this functional impairment remain unclear.
Purpose of the Study:
- To review current knowledge on electrophysiological alterations, ion channel effects, neurotransmission, and neurotoxicity in rabies virus infection.
- To explore the potential role of neuronal apoptosis in rabies pathogenesis.
- To discuss the relevance of observed apoptosis to natural rabies.
Main Methods:
- Literature review of electrophysiological alterations.
- Review of studies on ion channels and neurotransmission.
- Analysis of research on neurotoxicity and neuronal apoptosis in rabies virus infection.
Main Results:
- Rabies virus infection leads to neuronal dysfunction.
- Electrophysiological alterations, ion channel effects, and neurotoxicity are implicated in disease severity.
- Rabies virus can induce neuronal apoptosis in vitro and in vivo, though its significance in natural rabies is not fully established.
Conclusions:
- Neuronal dysfunction, rather than mild morphologic changes, is the likely cause of severe rabies.
- Apoptosis is a potential mechanism for rabies-induced neuronal death.
- Further research is needed to clarify the role of neuronal apoptosis in the pathogenesis of natural rabies.