Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

A novel population of myeloid cells responding to coxsackievirus infection assists in the dissemination of virus within the neonatal cns

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Tabor-Godwin, J. M.
  • Ruller, C. M.
  • Bagalso, N.
  • An, N.
  • Pagarigan, R. R.
  • Harkins, S.
  • Gilbert, P. E.
  • Kiosses, W. B.
  • Gude, N. A.
  • Cornell, C. T.
  • Doran, K. S.
  • Sussman, M. A.
  • Whitton, J. Lindsay
  • Feuer, Ralph

publication date

  • June 2010

journal

  • Journal of Neuroscience  Journal

abstract

  • Enterovirus infection in newborn infants is a significant cause of aseptic meningitis and encephalitis. Using a neonatal mouse model, we previously determined that coxsackievirus B3 (CVB3) preferentially targets proliferating neural stem cells located in the subventricular zone within 24 h after infection. At later time points, immature neuroblasts, and eventually mature neurons, were infected as determined by expression of high levels of viral protein. Here, we show that blood-derived Mac3(+) mononuclear cells were rapidly recruited to the CNS within 12 h after intracranial infection with CVB3. These cells displayed a myeloid-like morphology, were of a peripheral origin based on green fluorescent protein (GFP)-tagged adoptive cell transplant examination, and were highly susceptible to CVB3 infection during their migration into the CNS. Serial immunofluorescence images suggested that the myeloid cells enter the CNS via the choroid plexus, and that they may be infected during their extravasation and passage through the choroid plexus epithelium; these infected myeloid cells ultimately penetrate into the parenchyma of the brain. Before their migration through the ependymal cell layer, a subset of these infected myeloid cells expressed detectable levels of nestin, a marker for neural stem and progenitor cells. As these nestin(+) myeloid cells infected with CVB3 migrated through the ependymal cell layer, they revealed distinct morphological characteristics typical of type B neural stem cells. The recruitment of these novel myeloid cells may be specifically set in motion by the induction of a unique chemokine profile in the CNS induced very early after CVB3 infection, which includes upregulation of CCL12. We propose that intracranial CVB3 infection may lead to the recruitment of nestin(+) myeloid cells into the CNS which might represent an intrinsic host CNS repair response. In turn, the proliferative and metabolic status of recruited myeloid cells may render them attractive targets for CVB3 infection. Moreover, the migratory ability of these myeloid cells may point to a productive method of virus dissemination within the CNS.

subject areas

  • Animals
  • Animals, Newborn
  • Choroid Plexus
  • Coxsackievirus Infections
  • Fluorescent Antibody Technique
  • In Situ Hybridization
  • Mice
  • Microscopy, Confocal
  • Myeloid Cells
  • Neurons
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stem Cells
scroll to property group menus

Identity

PubMed Central ID

  • PMC2902258

International Standard Serial Number (ISSN)

  • 0270-6474

Digital Object Identifier (DOI)

  • 10.1523/jneurosci.1860-10.2010

PubMed ID

  • 20573913
scroll to property group menus

Additional Document Info

start page

  • 8676

end page

  • 8691

volume

  • 30

issue

  • 25

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support