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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form of EF-1delta significantly increases in cells infected with the recombinant HSV-1 in which UL13 had been replaced by HCMV UL97, a homologue of UL13.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.



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