Project description:human primary monocytes purified from 2 healthy blood donors were infected in vitro with Zika virus or HIV for 48 hours. Proteomics profiling of infected versus non infected cells was performed to identify up/down-regulated proteins associated to the infection
Project description:Genome wide DNA methylation profiling of monocytes from insulin sensitive and insulin resistant HIV-infected patients. The Illumina Infinium Human Methylation 450k Beadchip was used to obtain DNA methylation profiling across 450,000+ CpGs. Samples included monocytes from 37 HIV-infected individuals, of which 14 were insulin resistant and 23 were insulin sensitive, monocytes from 9 HIV-seronegative individuals, of which 4 were insulin sensitive and 5 insulin resistant, and FACS monocyte subsets (classical, intermediate, and non-classical monocytes) from two healthy donors.
Project description:Human cytomegalovirus induces a pro-inflammatory monocyte following infection. To begin to address how HCMV induces these rapid changes in infected monocytes, we examined the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of pro-inflammatory genes were upregulated within 4 hours post infection. Experiment Overall Design: To begin to globally define the HCMV-induced changes in monocyte function, we performed a transcriptome analysis. 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. A total of 6 replicates from mock-infected and 6 replicates from HCMV-infected monocytes were analyzed in this study.
Project description:Human cytomegalovirus induces a pro-inflammatory monocyte following infection. To begin to address how HCMV induces these rapid changes in infected monocytes, we examined the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of pro-inflammatory genes were upregulated within 4 hours post infection. Keywords: Disease State
Project description:Human cytomegalovirus (HCMV) induces pro-inflammatory monocytes following infection and we have evidence that EGFR is a key mediator in this early activation. To begin to address how this signalling pathway is responsible for the rapid activation of infected monocytes, we examined the role this pathway 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 EGFR-dependent manner, identifying this pathway as a key cellular control point in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection. Keywords: Disease state To begin to globally define how EGFR is involved in the HCMV-induced changes in monocyte function, we performed a transcriptome analysis in the presence of inhibitors to the EGFR signalling pathway. Specifically, a cDNA microarray containing 12,625 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 24 hours post infection in the presence of blocking anti-EGFR antibody and pharmacological agent AG1478 (AG; an EGFR inhibitor). A total of 4 replicates from mock-infected, HCMV-infected, anti-EGFR antibody-pretreated infected and AG-pretreated infected monocytes were analyzed in this study.
Project description:Human cytomegalovirus (HCMV) induces pro-inflammatory monocytes following infection and we have evidence that phosphatidylinositol 3-kinase [PI(3)K] is a key mediator in this activation. To begin to address how this signalling pathway is responsible for the functional changes in infected monocytes, we examined the role this pathway played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of genes were regulated in a PI(3)K-dependent manner, identifying this pathway as a key cellular control point in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection. Keywords: Disease state To begin to globally define how PI(3)K is involved in the HCMV-induced changes in monocyte function, we performed a transcriptome analysis in the presence of an inhibitor to the PI(3)K signalling pathway. Specifically, a cDNA microarray containing 12,626 unique probe sets was utilized to assess the modulation of the monocyte transcriptome at 48 hours post-infection in the presence of the pharmacological agent LY294002 (LY), a PI(3)K inhibitor. A total of 2 replicates from HCMV-infected monocytes, 2 replicates from LY-pretreated infected monocytes, and 2 replicates from mock-infected monocytes were analyzed in this study.