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Related Concept Videos

Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

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Related Experiment Video

Updated: Jun 21, 2026

Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
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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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Forebrain Neural Precursor Cells Are Differentially Vulnerable to Zika Virus Infection.

Samantha M Shelton1,2, Alexandra R Soucy3, Ronni Kurzion1

  • 1Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118.

Eneuro
|July 17, 2021
PubMed
Summary
This summary is machine-generated.

Zika virus (ZIKV) infection during pregnancy causes microcephaly. Researchers identified specific brain cells initially infected by ZIKV and found that AXL receptor expression influences cell vulnerability, aiding congenital Zika syndrome prevention.

Keywords:
Zikacorticogenesisdevelopmentheterogeneitymicrocephalyradial glia

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Zika Virus Infection of Cultured Human Fetal Brain Neural Stem Cells for Immunocytochemical Analysis
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Zika Virus Infection of Cultured Human Fetal Brain Neural Stem Cells for Immunocytochemical Analysis
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Zika Virus Infection of Cultured Human Fetal Brain Neural Stem Cells for Immunocytochemical Analysis

Published on: February 5, 2018

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Area of Science:

  • Neuroscience
  • Virology
  • Developmental Biology

Background:

  • Prenatal Zika virus (ZIKV) exposure can lead to microcephaly and congenital Zika syndrome.
  • The specific mechanisms and cellular targets of ZIKV in the developing fetal brain remain incompletely understood.
  • Identifying initially infected or spared cell populations is crucial for understanding ZIKV's neuropathogenesis.

Purpose of the Study:

  • To establish a murine model for studying fetal ZIKV infection.
  • To determine the temporal dynamics of ZIKV infection in the developing brain.
  • To identify specific cell types initially infected or resistant to ZIKV and elucidate factors contributing to heterogeneous vulnerability.

Main Methods:

  • Development of a novel murine model using intraventricular ZIKV infection and in utero electroporation (IUE).
  • In vivo time-course analysis of ZIKV infection in fetal brains.
  • Genetic fate mapping utilizing single-cell RNA sequencing (scRNAseq) data to identify cell-type-specific gene expression, including the ZIKV entry receptor AXL.

Main Results:

  • ZIKV was detected in apical radial glial cells (aRGCs) early post-infection, with basal intermediate progenitor cells (bIPCs) showing maximal infection after 3 days.
  • Microcephaly was observed as early as 1 day post-infection, attributed to apoptosis and reduced proliferation persisting until birth.
  • A subset of aRGCs expressing the AXL receptor demonstrated higher vulnerability to ZIKV infection compared to aRGCs with low AXL expression.

Conclusions:

  • The study provides a detailed temporal and cellular profile of ZIKV infection in the fetal brain using a novel murine model.
  • Heterogeneous vulnerability of aRGCs to ZIKV is linked to differential expression of the AXL receptor.
  • These findings offer critical insights for developing ZIKV prevention strategies and managing congenital Zika syndrome.