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Impaired Autophagy Flux is Associated with Proinflammatory Microglia Activation Following Japanese Encephalitis Virus

Alok Kumar1, J Kalita2, Rohit A Sinha3

  • 1Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareily Road, Lucknow, 226014, Uttar Pradesh, India. dralokkumar03@gmail.com.

Neurochemical Research
|July 3, 2020
PubMed

Insights

Japanese encephalitis virus (JEV) infection inhibits autophagy flux, leading to microglia activation, neuroinflammation, and neuronal death. This study reveals autophagy

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • The role of autophagy in Japanese encephalitis virus (JEV) infection remains largely unexplored.
  • Understanding cellular mechanisms is crucial for JEV pathogenesis.

Purpose of the Study:

  • To investigate the role of autophagy flux in microglia activation, neuroinflammation, and neuronal death during JEV infection.
  • To elucidate the impact of JEV on autophagy pathways and neuronal integrity.

Main Methods:

  • Utilized a mouse model of JEV infection.
  • Analyzed autophagy markers (LC3-II/I, SQSTM1/P62), neuronal death markers (caspase 12, H2Ax), and cathepsin D activity.
  • Assessed microglia activation, pro-inflammatory cytokines (IL1β, TNF-α, IFNγ, IL6), and neurobehavioral function.
  • Employed BV2-microglia and N2a-neuronal cell lines for in vitro studies.

Main Results:

  • JEV infection led to increased autophagy markers (LC3-II/I, SQSTM1/P62) and decreased cathepsin D activity by day 7.
  • Activated microglia exhibited elevated pro-inflammatory cytokine expression and increased DNA damage (H2AX) and neuronal cell death.
  • Neurobehavioral dysfunction and neuronal cell death pathways were observed in the hippocampus.
  • Inhibition of autophagy flux and neuronal cell death were consistent in N2a neuronal cells post-JEV infection.

Conclusions:

  • JEV infection disrupts autophagy flux, contributing to microglial activation and neuroinflammation.
  • Autophagy dysregulation plays a significant role in JEV-mediated neurodegeneration.
  • Findings highlight autophagy modulation as a potential therapeutic target for JEV infection.
Keywords:
AutophagyJapanese encephalitis virus infectionMicroglia activationNeuronal cell death

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