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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
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
HerpesHerpes simplexHerpes simplex encephalitis (HSE)Immune-mediated mechanismsRelapse

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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.