JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 Kawaguchi, Y.
Right arrow Articles by Hirai, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawaguchi, Y.
Right arrow Articles by Hirai, K.

 Previous Article  |  Next Article 

Journal of Virology, May 1999, p. 4456-4460, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Cellular Elongation Factor 1delta Is Modified in Cells Infected with Representative Alpha-, Beta-, or Gammaherpesviruses

Yasushi Kawaguchi,1 Tomio Matsumura,2 Bernard Roizman,3 and Kanji Hirai1,*

Department of Tumor Virology, Division of Virology and Immunology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510,1 and Epizootic Research Station, Equine Research Institute, Japan Racing Association, 1400-4, Shiba, Kokubunji-machi, Shimotsuga-gun, Tochigi 329-0412,2 Japan, and The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago, Illinois 606373

Received 16 November 1998/Accepted 1 February 1999

Earlier reports (Y. Kawaguchi, R. Bruni, and B. Roizman, J. Virol. 71:1019-1024, 1997; Y. Kawaguchi, C. Van Sant, and B. Roizman, J. Virol. 72:1731-1736, 1998) showed that herpes simplex virus 1 (HSV-1) infection causes the hyperphosphorylation of translation elongation factor 1delta (EF-1delta ) and that the modification of EF-1delta is the consequence of direct phosphorylation by a viral protein kinase encoded by the UL13 gene of HSV-1. The UL13 gene is conserved in members of all herpesvirus subfamilies. Here we report the following. (i) In various mammalian cells, accumulation of the hyperphosphorylated form of EF-1delta is observed after infection with alpha-, beta-, and gammaherpesviruses, including HSV-2, feline herpesvirus 1, pseudorabiesvirus, bovine herpesvirus 1, human cytomegalovirus (HCMV), and equine herpesvirus 2. (ii) In human lung fibroblast cells infected with recombinant HSV-1 lacking the UL13 gene, the hypophosphorylated form of EF-1delta is a minor species, whereas the amount of the hyperphosphorylated form of EF-1delta significantly increases in cells infected with the recombinant HSV-1 in which UL13 had been replaced by HCMV UL97, a homologue of UL13. These results indicate that the posttranslational modification of EF-1delta is conserved herpesvirus function and the UL13 homologues may be responsible for the universal modification of the translation factor.

* Corresponding author. Mailing address: Department of Tumor Virology, Division of Virology and Immunology, Medical Research Institute, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Phone: 81-3-5803-5814. Fax: 81-3-5803-0241. E-mail: hirai.creg{at}mri.tmd.ac.jp.

Journal of Virology, May 1999, p. 4456-4460, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



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

Copyright © 1999 by the American Society for Microbiology. All rights reserved.