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Journal of Virology, May 2009, p. 4316-4325, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02075-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Presence of p53 Influences the Expression of Multiple Human Cytomegalovirus Genes at Early Times Postinfection{triangledown}

Holger Hannemann, Kyle Rosenke, John M. O'Dowd, and Elizabeth A. Fortunato*

Department of Microbiology, Molecular Biology, and Biochemistry and Center for Reproductive Biology, University of Idaho, Moscow, Idaho

Received 2 October 2008/ Accepted 6 February 2009

Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunocompromised and immunosuppressed individuals. During infection, HCMV is known to employ host transcription factors to facilitate viral gene expression. To further understand the previously observed delay in viral replication and protein expression in p53 knockout cells, we conducted microarray analyses of p53+/+ and p53–/– immortalized fibroblast cell lines. At a multiplicity of infection (MOI) of 1 at 24 h postinfection (p.i.), the expression of 22 viral genes was affected by the absence of p53. Eleven of these 22 genes (group 1) were examined by real-time reverse transcriptase, or quantitative, PCR (q-PCR). Additionally, five genes previously determined to have p53 bound to their nearest p53-responsive elements (group 2) and three control genes without p53 binding sites in their upstream sequences (group 3) were also examined. At an MOI of 1, >3-fold regulation was found for five group 1 genes. The expression of group 2 and 3 genes was not changed. At an MOI of 5, all genes from group 1 and four of five genes from group 2 were found to be regulated. The expression of control genes from group 3 remained unchanged. A q-PCR time course of four genes revealed that p53 influences viral gene expression most at immediate-early and early times p.i., suggesting a mechanism for the reduced and delayed production of virions in p53–/– cells.

* Corresponding author. Mailing address: Department of Microbiology, Molecular Biology, and Biochemistry and the Center for Reproductive Biology, University of Idaho, Moscow, ID 83844-3052. Phone: (208) 885-6966. Fax: (208) 885-6518. E-mail: lfort{at}uidaho.edu

{triangledown} Published ahead of print on 18 February 2009.

Journal of Virology, May 2009, p. 4316-4325, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02075-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hwang, E.-S., Zhang, Z., Cai, H., Huang, D. Y., Huong, S.-M., Cha, C.-Y., Huang, E.-S. (2009). Human Cytomegalovirus IE1-72 Protein Interacts with p53 and Inhibits p53-Dependent Transactivation by a Mechanism Different from That of IE2-86 Protein. J. Virol. 83: 12388-12398 [Abstract] [Full Text]  


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