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Journal of Virology, June 2009, p. 5835-5845, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.00219-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Regulation of Histone Deposition on the Herpes Simplex Virus Type 1 Genome during Lytic Infection{triangledown} ,{dagger}

Sebla B. Kutluay1,3 and Steven J. Triezenberg1,2,3*

Graduate Program in Cell and Molecular Biology,1 Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824,2 Van Andel Research Institute, Grand Rapids, Michigan 495033

Received 30 January 2009/ Accepted 18 March 2009

During lytic infection by herpes simplex virus type 1 (HSV-1), histones are present at relatively low levels on the viral genome. However, the mechanisms that account for such low levels—how histone deposition on the viral genome is blocked or how histones are removed from the genome—are not yet defined. In this study, we show that histone occupancy on the viral genome gradually increased with time when transcription of the viral immediate-early (IE) genes was inhibited either by deletion of the VP16 activation domain or by chemical inhibition of RNA polymerase II (RNAP II). Inhibition of IE protein synthesis by cycloheximide did not affect histone occupancy on most IE promoters and coding regions but did cause an increase at delayed-early and late gene promoters. IE gene transcription from HSV-1 genomes associated with high levels of histones was stimulated by superinfection with HSV-2 without altering histone occupancy or covalent histone modifications at IE gene promoters. Moreover, RNAP II and histones cooccupied the viral genome in this context, indicating that RNAP II does not preferentially associate with viral genomes that are devoid of histones. These results suggest that during lytic infection, VP16, RNAP II, and IE proteins may all contribute to the low levels of histones on the viral genome, and yet the dearth of histones is neither a prerequisite for nor a necessary result of VP16-dependent transcription of nucleosomal viral genomes.

* Corresponding author. Mailing address: Van Andel Research Institute, 333 Bostwick NE, Grand Rapids, MI 49503. Phone: (616) 234-5704. Fax: (616) 234-5709. E-mail: steve.triezenberg{at}vai.org

{triangledown} Published ahead of print on 25 March 2009.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, June 2009, p. 5835-5845, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.00219-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Lacasse, J. J., Schang, L. M. (2010). During Lytic Infections, Herpes Simplex Virus Type 1 DNA Is in Complexes with the Properties of Unstable Nucleosomes. J. Virol. 84: 1920-1933 [Abstract] [Full Text]  


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