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Related Experiment Video

Updated: Apr 23, 2026

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SARS-CoV-2 Spike Protein S1 Subunit Induces Neuroinflammation Via Microglial Kv1.3 Channel.

Hee-Yoon Lee1, Young Lee1, Su-Hyun Jo2

  • 1Department of Physiology, Dental Research Institute, Seoul National University School of Dentistry, Seoul, South Korea.

Biological Psychiatry Global Open Science
|April 22, 2026
PubMed
Summary

The SARS-CoV-2 S1 protein activates microglia via Kv1.3 channels, causing neuroinflammation and anxiety. Chlorpromazine (CPZ) blocks this pathway, offering potential treatment for post-COVID conditions.

Keywords:
ChlorpromazineKv1.3 channelMicrogliaNeuroinflammationPost-COVID syndromeSARS-CoV-2 spike protein S1 subunit

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • Neuroinflammation is implicated in neurological disorders and post-COVID conditions.
  • The SARS-CoV-2 spike protein S1 subunit (S1 protein) activates microglia, but the mechanism is unclear.
  • Kv1.3 channels are identified as a key player in S1 protein-mediated neuroinflammation.

Purpose of the Study:

  • To elucidate the mechanism of S1 protein-induced microglial activation.
  • To investigate the role of Kv1.3 channels in S1 protein-mediated neuroinflammation.
  • To evaluate chlorpromazine (CPZ) as a potential therapeutic agent for S1 protein-induced neurological effects.

Main Methods:

  • Whole-cell patch clamp recordings of microglia in CX3CR1GFP/+ mice.
  • Iba1 immunohistochemistry and behavioral analyses were performed.
  • Assessed the effects of S1 protein and CPZ on Kv1.3 channel activity and microglial activation.

Main Results:

  • S1 protein increased Kv1.3 channel activity and microglial activation in the lateral septum, inducing behavioral changes.
  • CPZ inhibited S1 protein-mediated increases in Kv1.3 channel current and microglia size.
  • S1 protein induced anxiety-like behavior in mice, which was alleviated by CPZ.

Conclusions:

  • The Kv1.3 channel is a critical mediator of S1 protein-induced neuroinflammation and associated behavioral changes.
  • CPZ demonstrates potential as a therapeutic intervention for neurological symptoms associated with SARS-CoV-2 infection.
  • This study provides molecular insights into post-COVID neurological conditions and identifies a potential treatment target.