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Journal of Virology, January 2009, p. 1009-1017, Vol. 83, No. 2
0022-538X/09/$08.00+0     doi:10.1128/JVI.02245-07
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

VP22 of Herpes Simplex Virus 1 Promotes Protein Synthesis at Late Times in Infection and Accumulation of a Subset of Viral mRNAs at Early Times in Infection{triangledown}

Carol Duffy,1 Ekaette F. Mbong,1 and Joel D. Baines2*

Department of Biological Sciences, The University of Alabama, Tuscaloosa, Alabama 35487,1 Department of Microbiology and Immunology, New York State College of Veterinary Medicine, Cornell University, Ithaca, New York 148532

Received 16 October 2007/ Accepted 24 October 2008

VP22, encoded by the UL49 gene, is one of the most abundant proteins of the herpes simplex virus 1 (HSV-1) tegument. In the present study we show VP22 is required for optimal protein synthesis at late times in infection. Specifically, in the absence of VP22, viral proteins accumulated to wild-type levels until ~6 h postinfection. At that time, ongoing synthesis of most viral proteins dramatically decreased in the absence of VP22, whereas protein stability was not affected. Of the individual proteins we assayed, VP22 was required for optimal synthesis of the late viral proteins gE and gD and the immediate-early protein ICP0 but did not have discernible effects on accumulation of the immediate-early proteins ICP4 or ICP27. In addition, we found VP22 is required for the accumulation of a subset of mRNAs to wild-type levels at early, but not late, times in infection. Specifically, the presence of VP22 enhanced the accumulation of gE and gD mRNAs until ~9 h postinfection, but it had no discernible effect at later times in infection. Also, VP22 did not significantly affect ICP0 mRNA at any time in infection. Thus, the protein synthesis and mRNA phenotypes observed with the UL49-null virus are separable with regard to both timing during infection and the genes affected and suggest separate roles for VP22 in enhancing the accumulation of viral proteins and mRNAs. Finally, we show that VP22's effects on protein synthesis and mRNA accumulation occur independently of mutations in genes encoding the VP22-interacting partners VP16 and vhs.

* Corresponding author. Mailing address: C5-132 Veterinary Education Center, Cornell University, Ithaca, NY 14853. Phone: (607) 253-3391. Fax: (607) 253-3384. E-mail: jdb11{at}cornell.edu

{triangledown} Published ahead of print on 5 November 2008.

Journal of Virology, January 2009, p. 1009-1017, Vol. 83, No. 2
0022-538X/09/$08.00+0     doi:10.1128/JVI.02245-07
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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