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Herpes simplex encephalitis is linked with selective mitochondrial damage; a post-mortem and in vitro study.

Małgorzata Wnęk1, Lorenzo Ressel2,3, Emanuele Ricci2,3

  • 1Brain Infections Group, Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, L69 7BE, UK.

Acta Neuropathologica
|July 27, 2016
PubMed
Summary

Herpes simplex virus type-1 encephalitis causes mitochondrial damage in the brain, leading to severe outcomes. The antibiotic minocycline protected mitochondria and cells in this study, suggesting a potential new treatment for brain inflammation.

Keywords:
Gene-expressionHerpes simplex virus encephalitisHumanMinocyclineMitochondria

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Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Mitochondrial Biology

Background:

  • Herpes simplex virus type-1 encephalitis (HSE) is a leading cause of viral encephalitis with severe consequences.
  • Mitochondrial dysfunction is implicated in HSV infection but its role in human brain pathogenesis is unclear.
  • Minocycline is known to protect mitochondria and reduce brain damage.

Purpose of the Study:

  • To investigate mitochondrial genome (MtDNA) transcript changes in human HSE brain tissue.
  • To determine if mitochondrial damage occurs in the human brain during HSE and its contribution to pathogenesis.
  • To evaluate minocycline's potential therapeutic effects on mitochondrial function in HSE.

Main Methods:

  • Genome-wide transcriptomic analysis of post-mortem HSE brain tissue and controls.
  • Immunohistochemical analysis of HSV-1 and mitochondrial protein (CO1) co-localization.
  • In vitro study using primary human astrocytes infected with HSV-1 to assess mitochondrial function and minocycline's effects.

Main Results:

  • HSE brain tissue showed significant reduction in MtDNA-encoded transcripts.
  • Inverse correlation observed between HSV-1 abundance and mitochondrial protein CO1.
  • In vitro models confirmed preferential mitochondrial dysfunction and demonstrated minocycline's protective effects on mitochondrial function and cell viability.

Conclusions:

  • Mitochondrial damage is a critical and early event in HSV-1 encephalitis pathogenesis.
  • Minocycline preserves mitochondrial function and cell viability during HSV-1 infection.
  • Minocycline represents a potential adjunctive therapy for HSE to mitigate brain damage.