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Potential mechanisms of Zika‐linked microcephaly

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A recent outbreak of Zika virus (ZIKV) in Brazil is associated with microcephaly in infants born of infected mothers. As this pandemic spreads, rapid scientific investigation is shedding new light on how prenatal infection with ZIKV causes microcephaly. In this analysis we provide an overview of both microcephaly and ZIKV, explore the connection between prenatal ZIKV infection and microcephaly, and highlight recent insights into how prenatal ZIKV infection depletes the pool of neural progenitors in the developing brain.

(a) The human cortex develops and grows primarily from two populations of neural stem cells—radial glia [RG; light purple soma with dark purple nucleus positioned near the ventricle in the ventricular zone (VZ)] and outer radial glia [oRG; dark purple soma with light purple nucleus more basally located in the subventricular zone (SVZ)]. These cell types undergo self‐renewing asymmetric divisions, giving rise to either transit amplifying (intermediate progenitor) cells (dark purple) or postmitotic migratory neurons. (b) ZIKV preferentially targets proliferating neural cells including RG, oRG, and neural crest cells. It is likely that a combination of viral‐triggered apoptosis (left arrows) and precocious differentiation (right arrows) contribute to ZIKV‐liked microcephaly. Candidate receptors for Zika virions entry include a number of phosphotidylserine receptors (e.g., AXL, Mer, Tyro3, and TIM1) and are symbolized with a basic domain structure including Ig‐repeats (gray boxes) and kinase domains (green ovals). (Reprinted with permission from . Copyright 2016 The American Association for the Advancement of Science)
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Birth Defects > Craniofacial and Nervous System Anomalies
Adult Stem Cells, Tissue Renewal, and Regeneration > Stem Cells and Disease
Nervous System Development > Vertebrates: General Principles

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