JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] --
JVI Accepts, published online ahead of print on 5 March 2008
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.02763-07v1
82/10/4688    most recent
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 Google Scholar
Google Scholar
Right arrow Articles by Liang, L.
Right arrow Articles by Roizman, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liang, L.
Right arrow Articles by Roizman, B.

 Previous Article  |  Next Article 

J. Virol. doi:10.1128/JVI.02763-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The expression of interferon {gamma} dependent genes is blocked independently by the virion host shutoff RNase and by the US3 protein kinase

Li Liang and Bernard Roizman*

Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 East 58th Street, Chicago IL 60637

* To whom correspondence should be addressed. Email: bernard.roizman{at}bsd.uchicago.edu.


  Abstract

Interferon {gamma} receptor {alpha} (IFN{gamma}R{alpha}) is stable but posttranslationally modified in HSV-1(F) infected cells. Studies with antibody directed to the phosphorylation site indicate IFN{gamma}R{alpha} is phosphorylated by the US3 kinase. The modification is abolished in cells infected with {Delta}US3, DUL13 or {Delta}(US3/UL13) mutant viruses.. Transcripts of the IFN{gamma}-dependent genes do not accumulate in cells transduced with the US3 protein kinase and treated with interferon {gamma}. In contrast, the accumulation of IFN{gamma}-dependent gene transcripts is suppressed in wild-type virus infected cells, in cells infected with the {Delta}US3 mutant virus and to a lesser extent in the {Delta}UL41 virus-infected cells. The accumulation of IFN{gamma}-dependent gene transcripts in {Delta}UL41-infected cells could at least in part be due to a significant delay and reduction in the accumulation of the US3 protein. The results suggest that the expression of interferon {gamma}-dependent genes is blocked independently by the degradation of interferon {gamma}-dependent gene transcripts – a function of the virion host shutoff RNase, and by posttranslational modification of the IFN{gamma}R{alpha} protein.






Home Help [Feedback] [For Subscribers] [Archive] [Search] --
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2008 by the American Society for Microbiology. All rights reserved.