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West Nile virus neuroinvasive disease (WNND) causes memory loss by impairing hippocampal repair. Blocking interleukin-1 signaling in astrocytes restores neurogenesis and prevents cognitive deficits.

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • West Nile virus neuroinvasive disease (WNND) leads to persistent memory impairment due to hippocampal synapse loss.
  • Adult neurogenesis and synaptogenesis are crucial for hippocampal repair, processes potentially disrupted by viral infections.

Purpose of the Study:

  • To investigate the mechanisms by which WNND affects adult neurogenesis and synaptogenesis in the hippocampus.
  • To identify potential therapeutic targets for mitigating WNND-induced cognitive dysfunction.

Main Methods:

  • Transcriptional profiling of WNND-affected mouse models to identify gene expression changes.
  • Analysis of neurogenesis, astrogenesis, and cytokine production in isolated microglia and astrocytes.
  • Assessment of cognitive function and hippocampal repair in mice deficient in IL-1 receptor 1 (IL-1R1) or treated with an IL-1R1 antagonist.

Main Results:

  • WNND induced alterations in genes limiting neurogenesis, including interleukin-1 (IL-1).
  • Recovered mice showed reduced neurogenesis and increased astrogenesis, with impaired recovery of hippocampal neurogenesis.
  • Astrocytes were identified as the primary source of IL-1.
  • IL-1R1 deficiency or antagonism restored neurogenesis, synaptic recovery, and resistance to spatial learning deficits.

Conclusions:

  • Proinflammatory astrocytes impair neuronal progenitor cell homeostasis via IL-1, contributing to long-term cognitive deficits after WNND.
  • Targeting the IL-1 pathway, specifically IL-1R1, offers a potential therapeutic strategy for WNND-induced cognitive impairment.