Microglia depletion exacerbates demyelination and impairs remyelination in a neurotropic coronavirus infection

Alan Sariol1, Samantha Mackin2, Merri-Grace Allred1

  • 1Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242.

Insights

Microglia are crucial for clearing myelin debris and initiating repair after coronavirus infection. Their depletion impairs myelin repair and prolongs disease, highlighting their essential early-stage role in central nervous system recovery.

Area of Science:

  • Neuroimmunology
  • Neurovirology
  • Demyelinating Diseases

Background:

  • Microglia's dual role in demyelination recovery is poorly understood.
  • Understanding microglia's specific functions is critical for developing therapeutic strategies.

Purpose of the Study:

  • To elucidate the precise role of microglia in myelin repair following viral-induced demyelination.
  • To investigate the impact of microglia depletion on central nervous system recovery from neurotropic coronavirus infection.

Main Methods:

  • Utilized colony stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia in mice infected with mouse hepatitis virus (MHV).
  • Analyzed myelin repair, clinical disease progression, viral clearance kinetics, and oligodendrocyte numbers.
  • Performed gene expression analysis to identify molecular pathways involved in microglial function.

Main Results:

  • Microglia depletion during viral clearance impaired myelin repair and prolonged disease, without affecting virus clearance.
  • Large deposits of myelin debris were observed in treated mice, correlating with reduced oligodendrocyte numbers.
  • Gene expression revealed altered pathways for debris clearance, lipid recycling, and oligodendrocyte support; macrophages could not compensate for microglia loss.

Conclusions:

  • Microglia are essential for efficient myelin debris clearance and initiating remyelination after neurotropic coronavirus infection.
  • Microglial functions are critical during early remyelination stages but not required for later repair processes.
  • Infiltrating macrophages do not compensate for the loss of microglial functions in this model.