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Saving varicella from suicide

Saving varicella from suicide <h2>Saving varicella from suicide</h2> Intact VZV is released when trafficking to late endosomes is shut off in skin. GERSHON/ELSEVIER Varicella zoster virus (VZV) causes both varicella (chickenpox) and zoster (shingles). VZV spreads throughout the body, but it does so slowly, and virus only emerges extracellularly in the skin where it can spread to other hosts. That behavior is now explained by Zhenglun Zhu (Harvard Medical School, Boston, MA), Jason Chen, Anne Gershon, and Michael Gershon (Columbia University, New York, NY). They show that in most tissues VZV is diverted to late endosomes for destruction, but in the most superficial epidermal cells that cellular trafficking pathway is turned off, resulting in secretion of VZV. Trafficking from the Golgi system to the late endosome is mediated by the cation-independent mannose 6-phosphate receptor (MPR ci ). MPR ci has been implicated in both VZV entry (mannose 6-phosphate can block infection by free virus) and viral sorting (mature virus ends up in late endosomes). “The idea was around, based on indirect evidence, but it needed to be shown,” says Michael Gershon. The team tested the theory of MPR ci involvement by getting rid of MPR ci with antisense and siRNA. The resulting http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

Saving varicella from suicide

The Journal of Cell Biology , Volume 168 (3): 348 – Jan 31, 2005

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Publisher
Rockefeller University Press
Copyright
© 2005 Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb1683rr1
Publisher site
See Article on Publisher Site

Abstract

<h2>Saving varicella from suicide</h2> Intact VZV is released when trafficking to late endosomes is shut off in skin. GERSHON/ELSEVIER Varicella zoster virus (VZV) causes both varicella (chickenpox) and zoster (shingles). VZV spreads throughout the body, but it does so slowly, and virus only emerges extracellularly in the skin where it can spread to other hosts. That behavior is now explained by Zhenglun Zhu (Harvard Medical School, Boston, MA), Jason Chen, Anne Gershon, and Michael Gershon (Columbia University, New York, NY). They show that in most tissues VZV is diverted to late endosomes for destruction, but in the most superficial epidermal cells that cellular trafficking pathway is turned off, resulting in secretion of VZV. Trafficking from the Golgi system to the late endosome is mediated by the cation-independent mannose 6-phosphate receptor (MPR ci ). MPR ci has been implicated in both VZV entry (mannose 6-phosphate can block infection by free virus) and viral sorting (mature virus ends up in late endosomes). “The idea was around, based on indirect evidence, but it needed to be shown,” says Michael Gershon. The team tested the theory of MPR ci involvement by getting rid of MPR ci with antisense and siRNA. The resulting

Journal

The Journal of Cell BiologyRockefeller University Press

Published: Jan 31, 2005

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