This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reichelt, M.
Right arrow Articles by Arvin, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reichelt, M.
Right arrow Articles by Arvin, A. M.

 Previous Article  |  Next Article 

Journal of Virology, April 2008, p. 3971-3983, Vol. 82, No. 8
0022-538X/08/$08.00+0     doi:10.1128/JVI.02592-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Mechanisms of Varicella-Zoster Virus Neuropathogenesis in Human Dorsal Root Ganglia{triangledown}

Mike Reichelt,* Leigh Zerboni, and Ann M. Arvin

Departments of Pediatrics and Microbiology & Immunology, Stanford University School of Medicine, Stanford, California 94305

Received 5 December 2007/ Accepted 29 January 2008

Varicella-zoster virus (VZV) is a human alphaherpesvirus that infects sensory ganglia and reactivates from latency to cause herpes zoster. VZV replication was examined in human dorsal root ganglion (DRG) xenografts in mice with severe combined immunodeficiency using multiscale correlative immunofluorescence and electron microscopy. These experiments showed the presence of VZV genomic DNA, viral proteins, and virion production in both neurons and satellite cells within DRG. Furthermore, the multiscale analysis of VZV-host cell interactions revealed virus-induced cell-cell fusion and polykaryon formation between neurons and satellite cells during VZV replication in DRG in vivo. Satellite cell infection and polykaryon formation in neuron-satellite cell complexes provide mechanisms to amplify VZV entry into neuronal cell bodies, which is necessary for VZV transfer to skin in the affected dermatome during herpes zoster. These mechanisms of VZV neuropathogenesis help to account for the often severe neurologic consequences of herpes zoster.

* Corresponding author. Mailing address: Stanford University School of Medicine, 300 Pasteur Dr., Grant Bldg., Room S356, Stanford, CA 94305. Phone: (650) 723-6353. Fax: (650) 725-8040. E-mail: reichelt{at}stanford.edu

{triangledown} Published ahead of print on 6 February 2008.

Journal of Virology, April 2008, p. 3971-3983, Vol. 82, No. 8
0022-538X/08/$08.00+0     doi:10.1128/JVI.02592-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Reichelt, M., Brady, J., Arvin, A. M. (2009). The Replication Cycle of Varicella-Zoster Virus: Analysis of the Kinetics of Viral Protein Expression, Genome Synthesis, and Virion Assembly at the Single-Cell Level. J. Virol. 83: 3904-3918 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»