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Japanese Encephalitis Virus infection increases USP42 to stabilize TRIM21 and OAS1 for neuroinflammatory and

Ritu Mishra1, Kanhaiya Lal Kumawat2, Anirban Basu2

  • 1Laboratory of Virology, National Institute of Immunology, Aruna Asaf Ali Road, New Delhi, 110067, India.

Virology
|July 2, 2022
PubMed

Insights

Japanese Encephalitis Virus (JEV) infection decreases miR-590-3p, increasing USP42 levels. This elevates TRIM21 and OAS1, impacting neuroinflammation during Japanese encephalitis (JE).

Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Japanese encephalitis (JE) is a severe mosquito-borne viral disease caused by Japanese Encephalitis Virus (JEV).
  • Neuroinflammation, driven by dysregulated inflammatory responses, is a key factor in neuronal damage during JE.
  • Microglia play a critical role in the central nervous system's immune response to viral infections.

Purpose of the Study:

  • To investigate the role of microRNA-590-3p (miR-590-3p) in JEV infection within human microglial cells.
  • To elucidate the molecular mechanisms linking JEV infection, miR-590-3p, and downstream cellular targets involved in neuroinflammation.
  • To understand the interplay between USP42, TRIM21, and OAS1 in the context of JEV-induced microglial responses.

Main Methods:

  • Infection of human microglial cells (CHME3) with JEV.
  • Quantitative analysis of miR-590-3p, USP42, TRIM21, and OAS1 expression levels.
  • In vitro and in vivo experiments to assess protein stabilization and feedback loops.
  • Bioinformatic analysis to predict and confirm microRNA target interactions.

Main Results:

  • JEV infection significantly reduced cellular miR-590-3p levels in CHME3 cells.
  • miR-590-3p directly targets USP42, leading to increased USP42 expression upon JEV infection.
  • USP42 stabilizes TRIM21 via deubiquitination, maintaining higher cellular levels of TRIM21 and OAS1.
  • TRIM21 positively regulates USP42 levels, creating a feedback loop that further induces OAS1.

Conclusions:

  • JEV infection disrupts miR-590-3p regulation in human microglial cells.
  • The miR-590-3p/USP42/TRIM21/OAS1 axis is a critical pathway modulated during JEV infection.
  • Understanding this pathway provides insights into JEV pathogenesis and potential therapeutic targets for Japanese encephalitis.
Keywords:
DeubiquitinaseJapanese encephalitisMicrogliaNeuroinflammationmicroRNAs

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