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Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
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Postnatal Zika virus infection increases seizure susceptibility and disrupts cortical organization and GABAergic

Michele Ramos Lourenço1, Raissa Rilo Christoff2, Tailene Rabello2

  • 1Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, RJ, Brasil; Instituto Federal de Educação, Ciência e Tecnologia do Rio de Janeiro, RJ, Brasil.

Neuroscience
|September 3, 2025
PubMed

Insights

Zika virus (ZIKV) infection in mice disrupts the development of inhibitory GABAergic interneurons in the cerebral cortex. This developmental disruption is linked to increased seizure susceptibility and potential long-term neurological deficits.

Area of Science:

  • Neuroscience
  • Virology
  • Developmental Biology

Background:

  • Zika virus (ZIKV) infection during pregnancy causes severe fetal brain abnormalities, including microcephaly and cortical malformations.
  • Postnatal neurological issues like epilepsy and neurodevelopmental impairments are observed in infected infants.
  • While ZIKV's impact on glutamatergic neurons is studied, its effect on GABAergic interneurons, critical for brain circuitry and epilepsy, remains unclear.

Purpose of the Study:

  • To investigate the impact of perinatal ZIKV infection on the organization of cortical GABAergic interneurons during postnatal development into adulthood.
  • To assess ZIKV-induced alterations in neuronal activity and cortical structure in a mouse model.

Main Methods:

  • Perinatal infection of mice with Zika virus (ZIKV).
  • Evaluation of hyperthermic seizure susceptibility.
  • Assessment of c-Fos expression as a marker of neuronal activity.
  • Histological analysis (HE staining) for cortical disorganization and cell morphology.
  • Immunohistochemical analysis of GABAergic interneuron populations (calbindin-positive and parvalbumin-positive cells) at postnatal day 60.

Main Results:

  • ZIKV-infected pups exhibited increased susceptibility to hyperthermic seizures.
  • Elevated c-Fos expression indicated increased neuronal activity in the cerebral cortex of infected mice.
  • Histological examination revealed cortical disorganization and dysmorphic cells.
  • ZIKV infection led to altered positioning and distribution of calbindin- and parvalbumin-positive GABAergic interneurons compared to controls.

Conclusions:

  • Perinatal ZIKV infection disrupts the normal organization and distribution of cortical GABAergic interneurons.
  • These disruptions suggest impaired cortical inhibition following ZIKV infection.
  • The findings link ZIKV-induced neurodevelopmental alterations to an increased risk of hyperthermic seizures.

Keywords:
Brain developmentCongenital zika syndromeCortical malformationEpilepsyHyperthermic seizuresInhibitory neurons

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