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Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
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Nuclear accumulation of host transcripts during Zika Virus Infection.

Kristoffer E Leon1,2,3,4, Mir M Khalid1, Ryan A Flynn5,6

  • 1J. David Gladstone Institutes, San Francisco, California, United States of America.

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|January 5, 2023
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Summary

Zika virus (ZIKV) disrupts brain development by altering how neural progenitor cells (NPCs) manage RNA. This impacts UPF1 protein, leading to abnormal mRNA transport and reduced FREM2 protein, crucial for maintaining NPC identity.

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Area of Science:

  • Neuroscience
  • Virology
  • Molecular Biology

Background:

  • Zika virus (ZIKV) infection of fetal neural progenitor cells (NPCs) causes severe in utero neurodevelopmental disorders.
  • ZIKV disrupts multiple pathways essential for normal brain development, but the central mechanisms remain unclear.

Purpose of the Study:

  • To investigate how ZIKV infection reprograms host pathways in NPCs.
  • To identify the role of RNA-binding proteins in ZIKV-induced neurodevelopmental defects.

Main Methods:

  • Utilized infrared crosslinking immunoprecipitation and RNA sequencing (irCLIP-Seq) to analyze RNA-protein interactions.
  • Assessed mRNA subcellular localization and protein expression in ZIKV-infected NPCs and UPF1 knockdown models.

Main Results:

  • ZIKV infection diminishes the expression of UPF1, an RNA-binding protein, in NPCs.
  • A subset of host mRNAs showed reduced UPF1 binding and altered nuclear accumulation in ZIKV-infected or UPF1-depleted NPCs.
  • This mislocalization of specific mRNAs led to decreased expression of FREM2, a protein vital for NPC identity.

Conclusions:

  • ZIKV infection perturbs mRNA transport in NPCs by affecting UPF1 function.
  • The disruption of UPF1-mediated mRNA localization is a key mechanism by which ZIKV impairs neurodevelopment.