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The Host NADase CD38 Promotes JEV Replication by Targeting the NAD+/SIRT1 Axis.

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Japanese encephalitis virus (JEV) manipulates host metabolism by hijacking the CD38 enzyme. Blocking CD38 boosts NAD+ levels, inhibiting viral replication and offering a potential therapeutic strategy against JEV.

Keywords:
CD38Japanese encephalitis virusNAD+ metabolismSIRT1/p53 axis

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Area of Science:

  • Virology
  • Cellular Metabolism
  • Molecular Biology

Background:

  • Flaviviruses, including Japanese encephalitis virus (JEV), exploit host cellular metabolism for infection.
  • Understanding host-pathogen metabolic interactions is crucial for developing antiviral strategies.

Purpose of the Study:

  • To identify host factors regulating JEV-induced metabolic reprogramming.
  • To investigate the role of NADase CD38 in JEV infection and host defense.

Main Methods:

  • Utilized CRISPR/Cas9 technology to generate CD38 knockout (KO) TM3 cell lines.
  • Assessed viral particle production and entry in CD38-deficient cells.
  • Analyzed intracellular NAD+ levels, SIRT1 activity, and p53 status.
  • Employed pharmacological inhibitors and activators (EX527, SRT1720) to modulate the SIRT1 pathway.

Main Results:

  • CD38 deficiency significantly restricted infectious JEV particle production.
  • Loss of CD38 partially impaired viral entry but primarily enhanced host metabolic defense.
  • CD38 deficiency led to increased intracellular NAD+, sustained SIRT1 activity, and p53 inactivation, blocking apoptosis.
  • Pharmacological modulation of SIRT1 confirmed its role in regulating JEV replication.

Conclusions:

  • JEV hijacks the CD38-NAD+-SIRT1-p53 axis to suppress host metabolic defenses.
  • CD38 plays a critical role in promoting JEV infection by manipulating cellular metabolism.
  • CD38 represents a promising therapeutic target for JEV infection.