Human gene expression altered by Human cytomegalovirus (HCMV) Entry
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27974 | GEO | 2013/03/15
SECONDARY ACCESSION(S): PRJNA137769
REPOSITORIES: GEO
Similar Datasets
Project description:human foreskin fibroblasts were infected with HCMV We monitor cellular gene expression network altered by HCMV entry using Affymetrix Human Genome U133 Plus 2.0 Array 2 time points were measured, 5min, 25min
2013-03-15 | E-GEOD-27974 | biostudies-arrayexpress
Project description:We have established that human cytomegalovirus (HCMV) infection modulates the biology of target primary blood monocytes, allowing HCMV to use monocytes as 'vehicles' for its systemic spread. HCMV infection of monocytes results in rapid induction of PI(3)K and NF-kB activity. Integrins, which are upstream of the PI(3)K and NF-kB pathways, were shown to be involved in HCMV binding to and entry into fibroblasts, suggesting that receptor-ligand-mediated signaling following viral binding to integrins on monocytes could trigger the functional changes seen in infected monocytes. We now show that integrin engagement and the activation of the integrin/Src-signaling pathway is essential for the induction of HCMV-infected monocyte motility. To investigate how integrin engagement by HCMV triggers monocyte motility, we examined the infected monocyte transcriptome and found that the integrin/Src-signaling pathway regulates the expression of paxillin, which is an important signal transducer in the regulation of actin rearrangement during cell adhesion and movement. Functionally, we observed that paxillin is activated via the integrin/Src-signaling pathway and is required for monocyte motility. Because motility is intimately connected to cellular cytoskeletal organization, a process that is also important in viral entry, we investigated the role paxillin regulation plays in the process of viral entry of monocytes. New results confirmed that HCMV`s ability to enter target monocytes is significantly inhibited in cells deficient in paxillin expression or that had their integrin/Src/paxillin signaling pathway blocked. From our data, HCMV-cell interactions emerge as an essential trigger for the cellular changes that allow for HCMV entry and hematogenous dissemination. Monocytes were mock-infected, HCMV-infected, or pretreated with PP2 inhibitor prior to HCMV infection. There were three samples analyzed per individual replicate. Three replicates are included. comparative studies with a use of the specific Src kinase activity inhibitor
2010-10-31 | E-GEOD-24238 | biostudies-arrayexpress
Project description:We have established that human cytomegalovirus (HCMV) infection modulates the biology of target primary blood monocytes, allowing HCMV to use monocytes as “vehicles” for its systemic spread. HCMV infection of monocytes results in rapid induction of PI(3)K and NF-κB activity. Integrins, which are upstream of the PI(3)K and NF-κB pathways, were shown to be involved in HCMV binding to and entry into fibroblasts, suggesting that receptor-ligand-mediated signaling following viral binding to integrins on monocytes could trigger the functional changes seen in infected monocytes. We now show that integrin engagement and the activation of the integrin/Src-signaling pathway is essential for the induction of HCMV-infected monocyte motility. To investigate how integrin engagement by HCMV triggers monocyte motility, we examined the infected monocyte transcriptome and found that the integrin/Src-signaling pathway regulates the expression of paxillin, which is an important signal transducer in the regulation of actin rearrangement during cell adhesion and movement. Functionally, we observed that paxillin is activated via the integrin/Src-signaling pathway and is required for monocyte motility. Because motility is intimately connected to cellular cytoskeletal organization, a process that is also important in viral entry, we investigated the role paxillin regulation plays in the process of viral entry of monocytes. New results confirmed that HCMV`s ability to enter target monocytes is significantly inhibited in cells deficient in paxillin expression or that had their integrin/Src/paxillin signaling pathway blocked. From our data, HCMV-cell interactions emerge as an essential trigger for the cellular changes that allow for HCMV entry and hematogenous dissemination.
2010-10-31 | GSE24238 | GEO
Project description:We report the application of RNA sequencing for transcriptome analysis of HCMV infected Human nasal turbinate tissues, enabling the study of tissue responses to HCMV infection
2020-07-16 | GSE152114 | GEO
Project description:In this study, RNA-seq analysis was performed to generally understand the circRNA profiles of mock-infected and HCMV-infected HELF cells. Totally, 27,409 and 35,515 host circRNAs were identified in mock-infected and HCMV-infected HELF cells by RNA-seq respectively. Among them, 278 circRNAs were significantly modified filtrating by a threshold value of >2 (or <-2) fold-change and q-value <0.05. GO and KEGG pathway enrichment analysis suggested that the remarkably changed circRNAs might play important roles in viral entry, cell proliferation, and inhibition of apoptosis. Verification of four selected circRNAs ( circSP100, circMAP3K1, circTRIO, and circPLEKHM1) was performed using RT-PCR and Sanger sequencing. Moreover, further verification of circSP100 was performed using northern blotting and RT-qPCR and proteins binding directly to circSP100 were purified using RNA antisense purification (RAP).
2020-09-05 | GSE138836 | GEO
Project description:miRNA microarrays were used to investigate host miRNA expression profiles during HCMV clinical strain infection. Human foreskin fibroblasts (HFFs) were infected with the HCMV clinical strain Toledo. To mimic the attenuated strain, we used ToledoM-NM-^T15kb, which lacks the 15-kb genomic segment in the UL/bM-bM-^@M-^Y region. Changes in miRNA expression upon HCMV infection. Human foreskin fibroblasts (HFFs) were infected with Toledo-WT or ToledoM-NM-^T15kb for miRNA microarray (5 MOI). The miRNA expression levels of virus-infected HFFs at 24 or 72 hpi have been compared with those for the noninfected control.
2013-05-09 | E-GEOD-43761 | biostudies-arrayexpress
Project description:miRNA microarrays were used to investigate host miRNA expression profiles during HCMV clinical strain infection. Human foreskin fibroblasts (HFFs) were infected with the HCMV clinical strain Toledo. To mimic the attenuated strain, we used ToledoΔ15kb, which lacks the 15-kb genomic segment in the UL/b’ region.
2013-05-09 | GSE43761 | GEO
Project description:To elucidate miRNA-mediated temporal crosstalk during productive infection, we identified genome-wide miRNA target sites using Argonaute-crosslinking and immunoprecipitation followed by high-throughput sequencing (AGO-CLIPseq) in human cytomegalovirus (HCMV)-infected cells and evaluated the targeting efficacy by applying our new AGO-CLIPseq enrichment (ACE)-scoring algorithm. To uncover the miRNA targetome in uninfected or infected human foreskin fibroblasts with HCMV (24, 48 and 72 post-infection hour) were subjected to take AGO-CLIPseq as well as mRNAseq/smallRNAseq.
2014-12-03 | E-GEOD-63797 | biostudies-arrayexpress
Project description:We performed paired-end PRO-Seq and/or PRO-Cap on human foreskin fibroblasts (HFF) infected with human cytomegalovirus (HCMV) for 4 h (strain TB40/E) or 96 h (strain Towne varS). Each sample has matched uninfected controls. Towne experiments were also performed with adapters containing 4 nt of random sequence flanking both sides (8 total bases of randomness) to enable deduplication. Reads were first mapped to the human genome (hg38) (files available on GEO). Unmapped reads were then mapped to HCMV (Genbank FJ616285.1) (track hub available at https://github.com/P-TEFb/trackHub_HCMV).
2019-01-16 | GSE113394 | GEO
Project description:Primary human GBM stem like cells were infected with HCMV TR strain (MOI=1) and treated with IE siRNA (a combination of oligos targeting IE1 and IE2 HCMV genes) 72 hours following siRNA treatment, RNA was harvested using Qiagen and divided equally for profiling using Affymetrix arrays and HCMV arrays.
2015-08-13 | GSE56750 | GEO