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Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

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Myeloid cell interferon secretion restricts Zika flavivirus infection of developing and malignant human neural

Harry Bulstrode1, Gemma C Girdler1, Tannia Gracia2

  • 1Wellcome MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK; Division of Academic Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, UK.

Neuron
|September 29, 2022
PubMed

Insights

Zika virus infects developing brain cells, causing microcephaly. Glioblastoma cells, however, resist infection due to microglia-mediated innate immunity, offering potential for brain cancer therapies.

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • Zika virus (ZIKV) causes microcephaly by infecting human developing brain (HDB) progenitors.
  • Glioblastoma (GBM), an adult brain cancer, shares cellular tropism with HDB, suggesting therapeutic potential.
  • SOX2+ neural progenitors are present in both HDB and GBM tissues.

Purpose of the Study:

  • To compare ZIKV infection susceptibility in HDB and GBM primary tissue explants.
  • To investigate the role of innate immunity in ZIKV resistance in GBM.
  • To explore therapeutic strategies for ZIKV-induced microcephaly and GBM oncolysis.

Main Methods:

  • Primary tissue explants from HDB and GBM were infected with ZIKV.
  • SOX2+ GBM cell lines and HDB progenitor lines were utilized.
  • Conditioned medium from CD11b+ microglia/macrophages and type 1 interferon beta (IFNβ) were applied.
  • JAK1/2 signaling inhibition was employed to assess its effect on ZIKV infection.

Main Results:

  • HDB progenitors were uniformly vulnerable to ZIKV infection.
  • GBM tissues exhibited resistance to ZIKV, correlated with an innate immune signature.
  • GBM-derived CD11b+ microglia/macrophages conferred non-cell autonomous protection against ZIKV.
  • IFNβ, present in CD11b+-conditioned medium, induced resistance in both GBM and HDB progenitors.
  • JAK1/2 inhibition restored productive ZIKV infection in GBM progenitors.

Conclusions:

  • GBM-associated innate immunity, particularly from microglia/macrophages, protects neural progenitors from ZIKV.
  • IFNβ signaling is a key mechanism for ZIKV resistance in both developing and adult brain contexts.
  • These findings offer insights for neuroprotection strategies and enhancing oncolytic virotherapy for glioblastoma.
Keywords:
GBMZikaflavivirusglioblastomainterferonmacrophagemicrogliamyeloidneuraloncolytic

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