Flock house virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248687 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RNA-Seq analysis of the gene expression profile of wild type and dRassf mutant flies after infection by Flock House Virus
| PRJNA799124 | ENA
Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to Flock House virus (FHV) replicon induction.
2009-04-01 | GSE15467 | GEO
Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to infection with Flock House virus (FHV).
2009-04-01 | GSE15466 | GEO
Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to infection with Flock House virus (FHV). Experiment Overall Design: Cultured S2 cells were infected with FHV at an MOI of 10 and we measured global transcript levels at 12 h after infection compared to control mock infected cells using Affymetrix Drosophila Genome 1.0 microarray chips.
2009-04-11 | E-GEOD-15466 | biostudies-arrayexpress
Project description:How Management Practices within a Poultry House during Successive Flock Rotations Change the Structure of the Soil Microbiome
| PRJEB29406 | ENA
Project description:Frankliniella occidentalis strain:green house Transcriptome or Gene expression
| PRJNA252644 | ENA
Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to Flock House virus (FHV) replicon induction. Experiment Overall Design: Cultured S2 cells stably transfected with either a control replicon (pS2F1fs) or an FHV RNA1 replicon (pS2F1) were induced with 1 mM copper and we measured global transcript levels at 18 h after induction using Affymetrix Drosophila Genome 2.0 microarray chips.
2009-04-11 | E-GEOD-15467 | biostudies-arrayexpress
Project description:The larger segment (RNA 1) of the bipartite, positive-sense RNA genome of the nodavirus flock house virus encodes the viral RNA-dependent RNA polymerase. Two nonstructural viral proteins are made during the self-directed replication of this RNA: protein A (110 kDa), the translation product of RNA 1 itself, and protein B (11 kDa), the translation product of a subgenomic RNA (RNA 3) that is produced from RNA 1 during replication. To examine the roles of these proteins in RNA replication, specialized T7 transcription plasmids that contained wild-type or mutant copies of flock house virus RNA 1 cDNA were constructed and used in cells infected with the vaccinia virus-T7 RNA polymerase recombinant to make full-length transcripts that directed their own replication. Sequences in the primary transcripts that extended beyond the ends of the authentic RNA 1 sequence inhibited self-directed RNA replication, but plasmids that were constructed to minimize these terminal extensions produced primary transcripts that replicated as abundantly as authentic RNA 1. Truncation or mutation of the open reading frame for protein A eliminated self-directed replication, although the mutant RNA 1 remained a competent template for replication by wild-type protein A supplied in trans. These results showed that protein A was essential for RNA replication and that the process was not inseparably coupled to complete translation of the template. In contrast, protein B could be eliminated without inhibiting replication by mutations that disrupted the second of the two overlapping open reading frames on RNA 3. Furthermore, a mutant of RNA 1 in which the first nucleotide of the RNA 3 region was changed from G to U replicated at levels as high as those of the wild type without making either RNA 3 or protein B. However, diminishing replication levels were observed during subsequent replicative passages of RNA from both the mutants that could not make protein B. Roles for this protein that could account for the subtle phenotype of these mutants are discussed.
| S-EPMC188634 | biostudies-other
Project description:Little is known about the molecular determinants causing and sustaining viral persistent infections at the cellular level. We found that Drosophila cells persistently infected (PI) with Flock House virus (FHV) invariably harbor defective viral RNAs, which are replicated by the FHV RNA-dependent RNA polymerase. Some defective RNAs encoded a functional B2 protein, the FHV suppressor of RNA interference, which might contribute to maintenance of virus persistence. Viral small interfering RNAs (vsiRNAs) of both polarities were detected in PI cells and primarily mapped to regions of the viral genome that were preserved in the isolated defective RNAs. This indicated that defective RNAs could represent major sources of vsiRNAs. Immunofluorescence analysis revealed that mitochondria and viral proteins are differentially distributed in PI cells and lytically infected cells, which may partly explain the reduction in infectious viral progeny. Our results provide a basis for further investigations of the molecular mechanisms underlying persistent infections.
| S-EPMC3175792 | biostudies-literature