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A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation
Published on: April 2, 2012
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Herpes Simplex Encephalitis: an Update
John W Gnann1, Richard J Whitley2
1Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina, 135 Rutledge Avenue, MSC 752, Charleston, SC, 29425, USA. gnann@musc.edu.
Current Infectious Disease Reports
|March 3, 2017
Summary
Genetic defects in toll-like receptor 3 (TLR 3) pathways increase susceptibility to herpes simplex encephalitis (HSE). Early antiviral therapy improves outcomes, and distinguishing HSE from autoimmune encephalitis is crucial for treatment.
Area of Science:
- Neuroimmunology
- Infectious Diseases
- Genetics
Background:
- Herpes simplex encephalitis (HSE) is a severe neurological condition.
- Understanding its pathogenesis, diagnosis, and immune responses is critical for improving patient outcomes.
Purpose of the Study:
- To provide an update on current thinking regarding HSE.
- To emphasize new information on pathogenesis, diagnosis, and immune responses.
- To address genetic predisposition, clinical approaches for better outcomes, and immune-mediated mechanisms in relapsing HSE.
Main Methods:
- Review of recent findings on HSE pathogenesis, diagnosis, and immune responses.
- Analysis of genetic factors, clinical data, and immune mechanisms.
- Distinguishing HSE from autoimmune encephalitis.
Main Results:
- Genetic defects in toll-like receptor 3 (TLR 3) interferon pathways increase susceptibility to HSE.
- Early initiation of antiviral therapy significantly improves clinical outcomes.
- Many cases of "relapsing HSE" are actually anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis triggered by antecedent HSV infection.
- Exuberant immune responses during acute HSE may contribute to CNS pathology.
Conclusions:
- Innate immune responses and genetic factors play a role in HSE susceptibility.
- Prompt antiviral treatment is essential for favorable outcomes.
- Differentiating HSE from autoimmune NMDAR encephalitis is critical due to different therapeutic strategies.
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