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Nonfulminant herpes simplex encephalitis as a cause for mesial temporal sclerosis
M Schlitt1, A P Bucher, E A Quindlen
1Department of Neurosurgery, University of South Alabama Medical Center.
Abstract:
Although mesial temporal sclerosis has been recognized for more than 100 years, its etiology remains unknown. It is proposed that a common infectious agent, herpes simplex virus type-1, may cause this disorder by means of a nonfulminant infection of mesial temporal lobe structures, which is resolved by the immune system and becomes gliotic in the course of healing by the central nervous system. Brain sections from a long-term experiment in a model of herpes simplex encephalitis reveal such a scar, which shows a high concentration of glial fibrillary acidic protein, without any evidence of residual herpes antigen, by immunocytochemistry.
Insights
Herpes simplex virus type-1 may cause mesial temporal sclerosis through a resolved infection, leading to gliotic scarring in the brain. This study found evidence of glial scarring without residual viral antigens in a herpes encephalitis model.
Area of Science:
- Neurology
- Neurovirology
- Pathology
Background:
- Mesial temporal sclerosis (MTS) is a common neurological disorder with an unknown cause.
- The herpes simplex virus type-1 (HSV-1) is a potential, yet unproven, etiological agent for MTS.
Purpose of the Study:
- To investigate the hypothesis that HSV-1 infection can lead to the development of MTS.
- To identify potential pathological markers of HSV-1-induced MTS.
Main Methods:
- Utilized a long-term experimental model of herpes simplex encephalitis.
- Examined brain sections using immunocytochemistry to detect glial fibrillary acidic protein (GFAP) and herpes simplex viral antigens.
Main Results:
- Observed significant glial scarring, indicated by high GFAP concentration, in the mesial temporal lobe structures.
- Found no evidence of residual herpes simplex viral antigens in the affected brain areas.
Conclusions:
- The findings support the hypothesis that a resolved, nonfulminant HSV-1 infection could be an etiological factor in MTS.
- The observed glial scarring represents a central nervous system healing response to a past viral infection.