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Intracerebroventricular and Intravascular Injection of Viral Particles and Fluorescent Microbeads into the Neonatal Brain
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Published on: July 24, 2016

Coxsackievirus targets proliferating neuronal progenitor cells in the neonatal CNS

Ralph Feuer1, Robb R Pagarigan, Stephanie Harkins

  • 1Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 5, 2005
PubMed

Insights

Type B coxsackieviruses (CVB) infect developing brain stem cells in newborns, impairing their proliferation but not migration or differentiation. This viral neurotropism may explain fetal neurodevelopmental defects.

Area of Science:

  • Neurovirology
  • Developmental Neuroscience
  • Infectious Diseases

Background:

  • Type B coxsackieviruses (CVB) are a leading cause of viral meningitis.
  • Neonatal CVB infection poses risks for mortality and neurodevelopmental defects.
  • Previous studies identified CVB3 infection of neuronal progenitor cells in the subventricular zone (SVZ).

Purpose of the Study:

  • To investigate CVB3's cellular targets within the developing central nervous system (CNS).
  • To determine the impact of CVB3 infection on neural stem cell proliferation, migration, and differentiation.
  • To propose a model for CVB infection in the developing CNS.

Main Methods:

  • Utilized a mouse model of neonatal CVB infection.
  • Identified infected cells in the SVZ using proliferation markers (bromodeoxyuridine, Ki67).
  • Tracked migration and assessed differentiation of infected neuronal precursors.

Main Results:

  • CVB3 specifically targets actively proliferating stem cells (Type A and B) in the SVZ.
  • Infected cells lose proliferative capacity but retain migratory potential.
  • Infection does not inhibit neuronal precursor differentiation into mature cells.

Conclusions:

  • CVB3 infects and alters the behavior of neural stem and progenitor cells in the developing brain.
  • Despite impaired proliferation, infected cells migrate and differentiate, potentially contributing to neurodevelopmental abnormalities.
  • A model is proposed linking CVB infection of the developing CNS to observed defects.

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