Expression data from A549 cells infected by adenovirus not carrying virus associated sequences in the genome.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE58605 | GEO | 2014/09/01
SECONDARY ACCESSION(S): PRJNA253004
REPOSITORIES: GEO
Similar Datasets
Project description:Non-coding small RNAs are involved in viral life cycles. Adenovirus-encoding small RNAs, virus-associated RNAs (VA RNAs), are transcribed throughout the replication process, and the transcript levels depend on the copy numbers of the viral genome. Although the VA RNA transcription starts immediate early phase, little is known about the function in the early phase. Here we applied replication-deficient adenovirus vectors (AdVs) and novel VA-RNA deleted AdVs to analyze expression change of cellular gene mediated by VA RNAs. Human lung cell, A549, were infected by VA(+) or VA(-) adenoviral vectors. After the designed preiod of infection, cells were harvested and RNA was extacted, followed by DNA microarray analysis.
2014-09-01 | E-GEOD-58605 | biostudies-arrayexpress
Project description:The adenovirus (Ad) serotype 5 genome encodes two non-coding small RNAs (virus-associated RNAs: VA-RNAI and II), which are approximately 160nt-long RNAs transcribed by RNA polymerase III. Recent studies revealed that VA-RNAs are processed into VA-RNA-derived microRNAs (miRNAs) (mivaRNAI, II); however, we and another group recently demonstrated that mivaRNAI does not promote Ad replication. On the other hand, roles of VA-RNAII and VA-RNAII-derived miRNA (mivaRNAII) in Ad replication have remained to be clarified. In this study, we showed mivaRNAII-mediated promotion of Ad replication. Transfection with chemically synthesized 3'-mivaRNAII-138, one of the most abundant mivaRNAII, significantly enhanced Ad replication, while the other species of mivaRNAII did not. We used microarrays to detail gene expression profiles in HeLa cells transfected with 3'-miaRNAII-138 mimic and demonstarted that expression levels of various genes were down- or up-regulated following transfection with 3'-mivaRNAII-138 mimic.
2018-10-11 | GSE96531 | GEO
Project description:This Phase I/II trial evaluates LOAd703 in patients with cancer (pancreatic, biliary, colorectal or ovarian) together with their standard of care chemotherapy or using gemcitabine immune-conditioning. LOAd703 is administered by intratumoral image-guided injections. Maximum 50 patients can be enrolled.
LOAd703 is an immunostimulatory gene therapy using an selection replication competent adenovirus as a gene vehicle. The virus is derived from serotype 5 adenovirus with the fiber from serotype 35. It expresses the transgenes trimerized membrane-bound isoleucine zipper (TMZ) TMZ-CD40L and 41BBL under control of a cytomegalovirus (CMV) promoter.
| 2249969 | ecrin-mdr-crc
Project description:Adenovirus is a common human pathogen that relies on host cell processes for transcription and processing of viral RNA and protein production. Although adenoviral promoters, splice junctions, and cleavage and polyadenylation sites have been characterized using low-throughput biochemical techniques or short read cDNA-based sequencing, these technologies do not fully capture the complexity of the adenoviral transcriptome. By combining Illumina short-read and nanopore long-read direct RNA sequencing approaches, we mapped transcription start sites and cleavage and polyadenylation sites across the adenovirus genome. In addition to confirming the known canonical viral early and late RNA cassettes, our analysis of splice junctions within long RNA reads revealed an additional 35 novel viral transcripts. These RNAs include fourteen new splice junctions which lead to expression of canonical open reading frames (ORF), six novel ORF-containing transcripts, and fifteen transcripts encoding for messages that potentially alter protein functions through truncations or fusion of canonical ORFs. In addition, we also detect RNAs that bypass canonical cleavage sites and generate potential chimeric proteins by linking separate gene transcription units. Of these, an evolutionary conserved protein was detected containing the N-terminus of E4orf6 fused to the downstream DBP/E2A ORF. Loss of this novel protein, E4orf6/DBP, was associated with aberrant viral replication center morphology and poor viral spread. Our work highlights how long-read sequencing technologies can reveal further complexity within viral transcriptomes.
2022-08-30 | PXD034464 | Pride
Project description:We have identified desmoglein 2 (DSG2) as the primary high-affinity receptor used by adenovirus (Ad) serotypes Ad3, Ad7, and Ad14. These serotypes represent important human pathogens causing respiratory tract infections. In epithelial cells, adenovirus binding to DSG2 triggers events reminiscent of epithelial-to-mesenchymal transition, leading to transient opening of intercellular junctions. This improves access to receptors, e.g. CD46 and Her2/neu, that are trapped in intercellular junctions. In addition to complete virions, dodecahedral particles (PtDd) formed by viral penton and fiber in excess during viral replication, can trigger DSG2-mediated opening of intercellular junctions as shown by studies with recombinant Ad3 PtDd. Our findings shed light on adenovirus biology and pathogenesis and have implications for cancer therapy.
2010-12-08 | GSE24138 | GEO
Project description:We have identified desmoglein 2 (DSG2) as the primary high-affinity receptor used by adenovirus (Ad) serotypes Ad3, Ad7, and Ad14. These serotypes represent important human pathogens causing respiratory tract infections. In epithelial cells, adenovirus binding to DSG2 triggers events reminiscent of epithelial-to-mesenchymal transition, leading to transient opening of intercellular junctions. This improves access to receptors, e.g. CD46 and Her2/neu, that are trapped in intercellular junctions. In addition to complete virions, dodecahedral particles (PtDd) formed by viral penton and fiber in excess during viral replication, can trigger DSG2-mediated opening of intercellular junctions as shown by studies with recombinant Ad3 PtDd. Our findings shed light on adenovirus biology and pathogenesis and have implications for cancer therapy. 3 arrays, 3 experimental groups, 1 replicate in each group.
2010-12-08 | E-GEOD-24138 | biostudies-arrayexpress
Project description:Human adenovirus type 5 oncogene E1A was shown to induce massive re-replication of cellular DNA in late S phase. Using DNA combing analysis, it was shown that DNA replication dynamics including replicon length, fork velocity and inter-origin distance were dramatically altered in E1A expressing cells as compared to that of normal serum stimulated cells. It was also shown that c-Myc that is induced in E1A expressing cells is essential for the efficient entry of E1A expressing cells into S phase.
2013-05-22 | GSE47140 | GEO
Project description:To combat virus infections, which are major human killers, a deeper understanding of how viruses reprogram their hosts to create optimal production of progeny is needed. Most knowledge on the regulation of cellular gene expression during adenovirus infection is derived from studies of mRNA expression. Here, we investigated the changes in cellular protein expression during the early phase of adenovirus type 2 (Ad2) infection of primary human cells by stable isotope labeling in cell culture (SILAC) with subsequent liquid chromatography-high resolution tandem mass spectrometric (LC-MS/MS) analysis using a Q-Exactive Orbitrap instrument. Cells were in-depth evaluated 6 and 12 hours post infection (hpi) and two biological replicates were investigated using swapped labeling. In total, 2027 and 2150 proteins were quantified at 6 and 12 hpi, respectively. Among them, 431 and 544 were deregulated more than 1.5-fold at the two time points. For the deregulated proteins the change in protein expression was compared with that of late phase of infection (see PXD004095). Pathway analysis showed that De novo purine and pyrimidine biosynthesis, Glycolysis and Cytoskeletal regulation by Rho GTPase pathways are activated early during the infection, while the inactivation of the Integrin signalling pathway starts between 6 and 12 hpi. The transcription factor MYC was predicted to be activated with time, and the phosphopeptide analysis revealed the up-regulation of phosphosites related with glycolysis or cytoskeletal reorganization. These results complement the previous knowledge obtained from transcriptomic data, and show novel and specific aspects of how adenovirus influence host cell gene expression at the protein level.The results contribute to our understanding of host cell gene regulation during infection at a deeper level.
2018-10-04 | PXD008980 | Pride
Project description:As intracellular parasites, viruses exploit cellular proteins at every stage of infection. Adenovirus related outbreaks cause severe acute respiratory illnesses and conjunctivitis, with no specific antiviral therapy yet available. Herein, we investigate human adenovirus (HAdV-D37) pIIIa-host protein interactions by affinity purification and mass spectrometry (AP-MS) screens. We demonstrate that viral pIIIa interacts with ubiquitin-specific protease 9x (USP9x) and Ran-binding protein 2 (RANBP2). As intracellular parasites, viruses exploit cellular proteins at every stage of infection. Adenovirus related outbreaks cause severe acute respiratory illnesses and conjunctivitis, with no specific antiviral therapy yet available. Herein, we investigate human adenovirus (HAdV-D37) pIIIa-host protein interactions by affinity purification and mass spectrometry (AP-MS) screens. We demonstrate that viral pIIIa interacts with ubiquitin-specific protease 9x (USP9x) and Ran-binding protein 2 (RANBP2).
2022-05-30 | PXD023642 | Pride
Project description:Human adenovirus type 5 oncogene E1A was shown to induce massive re-replication of cellular DNA in late S phase. Using DNA combing analysis, it was shown that DNA replication dynamics including replicon length, fork velocity and inter-origin distance were dramatically altered in E1A expressing cells as compared to that of normal serum stimulated cells. It was also shown that c-Myc that is induced in E1A expressing cells is essential for the efficient entry of E1A expressing cells into S phase. Serum starved cells were infected with an adenovirus expressing only the transforming E1A protein, and with Adbeta-galactosidase (control) were analyzed by flow cytomery. DNA prepared from such cells were analyzed by DNA combing analysis and data obtained were examined statistically. Requirement of Myc in E1A induced S phase entry was also examined by using antisense Myc vector.
2013-05-22 | E-GEOD-47140 | biostudies-arrayexpress