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B- and Phosphatidylinositol 3-Kinase-Regulated Genes in Human Cytomegalovirus-Infected Monocytes
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Elizabeth R. Bivins-Smith,1,
M. Shane Smith,1 and
Andrew D. Yurochko1,2*
Department of Microbiology & Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932,1 Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center, Shreveport, Louisiana2
Received 23 April 2007/ Accepted 31 October 2007
Human cytomegalovirus induces a proinflammatory monocyte following infection, and we have evidence that NF-
B and phosphatidylinositol 3-kinase [PI(3)K] are key mediators in this early activation. To begin to address how these signaling pathways are responsible for the rapid activation of infected monocytes, we examined the role that these pathways played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed that a significant number of genes, including inflammatory genes, were regulated in an NF-
B- and/or PI(3)K-dependent manner, identifying the NF-
B and PI(3)K pathways as key cellular control points in the conversion of monocytes to an activated proinflammatory state following HCMV infection.
Published ahead of print on 14 November 2007.
Supplemental material for this article may be found at http://jvi.asm.org/.
These authors contributed equally to the work.
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