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Quantification of Antibody-dependent Enhancement of the Zika Virus in Primary Human Cells
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Quantification of Antibody-dependent Enhancement of the Zika Virus in Primary Human Cells

Published on: January 18, 2019

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Zika virus infected primary microglia impairs NPCs proliferation and differentiation

Jin Wang1, Jing Liu1, Rui Zhou1

  • 1State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, Nanjing Advanced Institute for Life Sciences (NAILS), School of Life Sciences, Nanjing University, Nanjing, Jiangsu, 210046, China.

Biochemical and Biophysical Research Communications
|February 18, 2018
PubMed

Insights

Zika virus (ZIKV) infection in microglia triggers neuroinflammation, impacting neural precursor cell (NPC) development. This suggests microglia-driven inflammation is key to ZIKV neuropathogenesis.

Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • Zika virus (ZIKV) causes severe birth defects like microcephaly by harming developing brains.
  • The specific role of microglia, the brain's immune cells, in ZIKV pathology remains unclear.
  • Understanding microglia-neural cell interactions is crucial for ZIKV neuropathogenesis.

Purpose of the Study:

  • To investigate the interaction between microglia and neural progenitor cells (NPCs) during ZIKV infection.
  • To elucidate the role of microglia-mediated immune responses in ZIKV-induced brain development impairment.

Main Methods:

  • Primary microglia were infected with ZIKV.
  • ZIKV-infected microglia-conditioned medium (CM) was used to treat mouse-derived NPCs.
  • Cytokine levels in CM were analyzed and blocked to assess their impact on NPC differentiation and proliferation.

Main Results:

  • ZIKV-infected microglia exhibited an inflammatory response, releasing high levels of TNF-α, IL-6, IL-1β, and iNOS.
  • CM from ZIKV-infected microglia inhibited NPC proliferation and neuronal differentiation.
  • Blocking cytokines in CM partially restored neurogenesis and reduced astrocytic differentiation.

Conclusions:

  • Microglia play a significant role in ZIKV neuropathogenesis through neuroinflammation.
  • Microglia-derived inflammatory mediators negatively impact neural progenitor cell development.
  • Targeting microglia-mediated inflammation may offer therapeutic strategies against ZIKV-induced neurological damage.
Keywords:
DifferentiationMicrogliaNeural precursor cellsNeuroinflammationProliferationZika virus

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