JCB logo
amgmicro.com
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 23 September 2002. doi:10.1083/jcb1587iti5
This Article
Right arrow Full Text (PDF, 294K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dove, A. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Dove, A. W.
Related Collections
Right arrowRelated Article
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

© The Rockefeller University Press, 0021-9525/2002/9/1153 $5.00
The Journal of Cell Biology, Volume 158, Number 7, September 30, 2002 1153-1153


In This Issue

Herpes spoils excitement


HSV-1 infection (bottom) prompts a loss of sodium channels (green).

People infected with the cold sore–causing herpes simplex virus 1 (HSV-1) often complain of abnormal sensations around the site of initial infection, a symptom apparently caused by the virus's ability to reduce the excitability of infected neurons. On page 1251, Storey et al. describe the molecular mechanism responsible for this phenomenon. Their findings may also be relevant to the normal rearrangements of voltage-dependent sodium channels that occur during neuronal development.

The authors found that neurons from the rat dorsal root ganglion show a profound and rapid loss of voltage-dependent sodium currents ~24 h after infection with HSV-1. Loss of excitability in these neurons correlates with the loss of sodium channels from the cell surface. Blocking endocytosis or preventing the production of HSV-1 late proteins prevents the loss of excitability, and a mutant virus lacking the neuro-virulence factor ICP 34.5 does not cause the loss of sodium channels seen in wild-type viral infections.Previous work has shown that HSV-1 modifies the ubiquitin–proteasome pathway, leading to the destruction of many cellular proteins, and this may also explain the internalization of sodium channels. If the virus is tapping into a normal cellular pathway, then the same ubiquitin–proteasome pathway may also explain the rapid disappearance of sodium channels at nodes of Ranvier during development. {blacksquare}



Alan W. Dove

alanwdove{at}earthlink.net


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?

Related Article

Selective internalization of sodium channels in rat dorsal root ganglion neurons infected with herpes simplex virus-1
Nina Storey, David Latchman, and Stuart Bevan
J. Cell Biol. 2002 158: 1251-1262. [Abstract] [Full Text] [PDF]




This Article
Right arrow Full Text (PDF, 294K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dove, A. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Dove, A. W.
Related Collections
Right arrowRelated Article
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?


  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents