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Journal of Virology, October 2003, p. 11006-11015, Vol. 77, No. 20
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.20.11006-11015.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Strategic Attack on Host Cell Gene Expression during Adenovirus Infection

Hongxing Zhao,1* Fredrik Granberg,1 Ludmila Elfineh,1 Ulf Pettersson,1 and Catharina Svensson2

Department of Genetics and Pathology, Rudbeck Laboratory, S-751 85 Uppsala,1 Department of Medical Biochemistry and Microbiology, Biomedical Centre, Uppsala University, S-741 23 Uppsala, Sweden2

Received 21 April 2003/ Accepted 14 July 2003

To understand the interaction between the virus and its host, we used three sources of cDNA microarrays to examine the expression of 12,309 unique genes at 6 h postinfection of HeLa cells with high multiplicities of adenovirus type 2. Seventy-six genes with significantly changed expression ratios were identified, suggesting that adenovirus only modulates expression of a limited set of cellular genes. Quantitative real-time PCR analyses on selected genes were performed to confirm the microarray results. Significantly, a pronounced transcriptional activation by the promiscuous E1A-289R transcriptional activator was not apparent. Instead, promoter sequences in 45% of the upregulated genes harbored a potential E2F binding site, suggesting that the ability of the amino-terminal domain of E1A to regulate E2F-dependent transcription may be a major pathway for regulation of cellular gene expression. CDC25A was the only upregulated gene directly involved in cell cycle control. In contrast, several genes implicated in cell growth arrest were repressed. The transforming growth factor beta superfamily was specifically affected in the expression of both the upstream ligand and an intracellular regulator. In agreement with previous reports, adenovirus also targeted the innate immune response by downregulating several cytokines, including CLL2, CXCL1, and interleukin-6. Finally, stress response genes encoding GADD45B, ATF3, and TP53AP1 were upregulated. Importantly, we also found a novel countermeasure—activation of the apoptosis inhibitor survivin.

* Corresponding author. Mailing address: Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden. Phone: 46 184714057. Fax: 46 18-471 4808. E-mail: Hongxing.Zhao{at}genpat.uu.se.

Journal of Virology, October 2003, p. 11006-11015, Vol. 77, No. 20
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.20.11006-11015.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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