BioProject

Human cytomegalovirus induces a pro-inflammatory monocyte following infection and we have evidence that NF-κB and phosphatidylinositol 3-kinase [PI(3)K] are key mediators in this early activation. More...

Human cytomegalovirus induces a pro-inflammatory monocyte following infection and we have evidence that NF-κB and phosphatidylinositol 3-kinase [PI(3)K] are key mediators in this early activation. To begin to address how these signalling pathways are responsible for the rapid activation of infected monocytes, we examined the role these pathways played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of genes, including inflammatory genes, were regulated in a NF-κB- and/or PI(3)K-dependent manner, identifying these pathways as key cellular control points in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection. Keywords: disease state analysis Overall design: To begin to globally define how NF-κB and PI(3)K are involved in the HCMV-induced changes in monocyte function, we performed a transcriptome analysis in the presence of inhibitors to NF-κB and PI(3)K signalling pathways. Specifically, a cDNA microarray containing 12,626 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 4 hours post infection in the presence of the pharmalogical agents Bay11-7082 (Bay11; a NF-κB inhibitor) and LY294002 (LY; a PI(3)K inhibitor). A total of 6 replicates from HCMV-infected monocytes, 3 replicates from Bay11-pretreated infected monocytes and 3 replicates from LY-pretreated infected monocytes were analyzed in this study. Less...