WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience Advertisement
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
The Journal of Neuroscience, March 2, 2005, 25(9):2434-2444; doi:10.1523/JNEUROSCI.4517-04.2005

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feuer, R.
Right arrow Articles by Whitton, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feuer, R.
Right arrow Articles by Whitton, J. L.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Stem Cells

 Previous Article  |  Next Article 

Neurobiology of Disease
Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Ralph Feuer, Robb R. Pagarigan, Stephanie Harkins, Fei Liu, Isabelle P. Hunziker, and J. Lindsay Whitton

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037

Type B coxsackieviruses (CVB) frequently infect the CNS and, together with other enteroviruses, are the most common cause of viral meningitis in humans. Newborn infants are particularly vulnerable, and CVB also can infect the fetus, leading to mortality, or to neurodevelopmental defects in surviving infants. Using a mouse model of neonatal CVB infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenitor cells in the subventricular zone (SVZ). Here we extend these findings, and we show that CVB3 targets actively proliferating (bromodeoxyuridine+, Ki67+) cells in the SVZ, including type B and type A stem cells. However, infected cells exiting the SVZ have lost their proliferative capacity, in contrast to their uninfected companions. Despite being proliferation deficient, the infected neuronal precursors could migrate along the rostral migratory stream and radial glia, to reach their final destinations in the olfactory bulb or cerebral cortex. Furthermore, infection did not prevent cell differentiation, as determined by cellular morphology and the expression of maturation markers. These data lead us to propose a model of CVB infection of the developing CNS, which may explain the neurodevelopmental defects that result from fetal infection.

Key words: migration; neuropathology; proliferation; infection; stem cells; coxsackievirus

Received Nov 3, 2004; revised December 20, 2004; accepted January 17, 2005.




This article has been cited by other articles:


Home page
 J. Virol.Home page
C. C. Kemball, S. Harkins, and J. L. Whitton
Enumeration and Functional Evaluation of Virus-Specific CD4+ and CD8+ T Cells in Lymphoid and Peripheral Sites of Coxsackievirus B3 Infection
J. Virol., May 1, 2008; 82(9): 4331 - 4342.
[Abstract] [Full Text] [PDF]


-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-