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A complement-microglial axis drives synapse loss during virus-induced memory impairment.

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  • 1Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.

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West Nile virus infection causes memory loss by triggering complement-mediated elimination of brain synapses. This study identifies a mechanism involving microglia and synaptic pruning in WNV survivors.

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • West Nile virus (WNV) neuroinvasive disease survivors often experience chronic cognitive deficits, particularly memory impairment.
  • The underlying mechanisms of WNV-induced memory dysfunction remain largely unknown.
  • The complement cascade, part of innate immunity, is known to mediate synaptic pruning during development.

Purpose of the Study:

  • To investigate the mechanisms of WNV-induced cognitive impairment.
  • To establish a murine model that recapitulates human WNV neuroinvasive disease and its sequelae.
  • To identify the role of the complement system and microglia in WNV-associated memory dysfunction.

Main Methods:

  • Utilized a WNV mutant (WNV-NS5-E218A) to model neuroinvasive disease in mice, mimicking human outcomes.
  • Assessed spatial learning, hippocampal pathology, microglial activity, and gene expression in recovered mice.
  • Examined complement component C1QA, presynaptic terminals, and microglial engulfment in WNV-infected and recovered murine and human samples.
  • Investigated the protective effects of microglial deficiency (Il34(-/-)) and complement pathway inhibition (C3 or C3a receptor deficiency).

Main Results:

  • WNV-NS5-E218A infection in mice resulted in impaired spatial learning and persistent phagocytic microglia post-recovery.
  • Increased expression of complement-driving genes was observed in hippocampi of mice with spatial memory deficits.
  • Loss of hippocampal CA3 presynaptic terminals was evident in both murine models and human post-mortem samples.
  • Microglial engulfment of presynaptic terminals occurred during acute infection and recovery.
  • Mice with reduced microglia or complement pathway deficiencies were protected from WNV-induced synaptic loss.

Conclusions:

  • A novel murine model for WNV-induced spatial memory impairment was developed.
  • Viral infection triggers complement-mediated elimination of presynaptic terminals in adult neurons.
  • This mechanism involving microglia and complement activation offers a potential explanation for neurocognitive impairments in WNV survivors.