Vaccinia virus strain:Copenhagen VVdelEdelK+RhTRS1
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ABSTRACT:
PROVIDER: PRJNA229414 | ENA |
REPOSITORIES: ENA
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Project description:Vaccinia virus evolution reveals adaptations to evade host viral nucleic acid sensing
| PRJNA271882 | ENA
Project description:High frequency single nucleotide changes and copy number amplification support rapid evolution of vaccinia virus
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Project description:Samples were received from the lab of Bertram Jacobs, experiments done by Jeff Langland (langland@asu.edu). Midlog Hela cells were infected with copenhagen strain Vaccinia Virus at MOI of 5. Viral stocks were sucrose pad purified. Incubated 2, 6, and 9 hrs post infection. viral mutants include VC2 (WT), VVdeltaE3L (e3L gene deleted), VVdelta83N(83N terminal amino acids of E3L delted, protein wont bind Z-DNA), VVdelta26C (26C terminal amino acids of E3L deleted, Protein wont bind dsRNA), VVdeltaE3l-ATV(E3L replaced with eIF2alpha homolog encoded by the salamander ATV virus. Product inhibits PKR but doesnt block IFN induction),and UV (UV inactivated WT)
2007-04-01 | E-TABM-64 | biostudies-arrayexpress
Project description:Orthopoxviruses are large DNA viruses which can cause disease in numerous host species. Even though the eradication of variola virus - the causative agent of human smallpox M-bM-^@M-^S succeeded, with the end of vaccinations several other orthopoxviruses emerged as potential threat to human health. For instance, animal-borne monkeypox virus, cowpox virus and closely related vaccinia virus are all capable of establishing zoonotic infections in humans. The disease caused by each virus differs in terms of expression and severity, but we still know little about the reasons for these different phenotypes. They may be explained by the unique repertoire of host cell modulating factors encoded by each virus. In this study, we aimed at characterizing the specific modulation of the host cells gene expression profile by orthopoxvirus infection. In our study we analyzed changes in host cell gene expression of HeLa cells after infection with cowpox virus, monkeypox virus or vaccinia virus and compared these to each other and to the gene expression profile of non-infected cells using Agilent Whole Genome Microarray technology. We could identify major differences in viral modulation of host cell immune response genes, especially an induction of genes involved in leukocyte migration and Toll-like receptor signalling in cowpox and monkeypox virus infected cells. This was not observed following vaccinia virus infection. If these differences contribute to the different clinical manifestation of cowpox, monkeypox and vaccinia virus infections in certain host species remains to be elucidated. We analyzed the gene expression profile of HeLa cells wich were either mock-infected or infected with Vaccinia virus strain IHD-W, Cowpox virus strain Brighton Red or Monkeypox virus strain MSF#6 at a multiplicity of infection of 5. Experiments were performed in duplicate. At 6 h post infection total RNA was isolated from infected cells and used for microarray analysis.
2012-04-14 | E-GEOD-36854 | biostudies-arrayexpress
Project description:Vaccinia virus Post replicative transcription start sites.
| PRJNA169009 | ENA
Project description:The purpose of this study is to determine the safety and maximum tolerated dose from injecting this vaccinia virus into tumors or infusion.
| 2047624 | ecrin-mdr-crc
Project description:Viral infection both activates stress signaling pathways and redistributes ribosomes away from host mRNAs to translate viral mRNAs. The intricacies of this ribosome shuffle from host to viral mRNAs are poorly understood Here, we uncover a role for the ribosome associated quality control (RQC) factor, ZNF598, during vaccinia virus mRNA translation. ZNF598 acts on collided ribosomes to ubiquitylate 40S subunit proteins uS10 and eS10 initiating RQC-dependent nascent chain degradation and ribosome recycling We show that vaccinia infection in human cells enhances uS10 ubiquitylation indicating an increased burden on RQC pathways during viral propagation. Consistent with an increased RQC demand, we demonstrate that vaccinia virus replication is impaired in cells which either lack ZNF598 or express a ubiquitylation deficient version of uS10 Using SILAC-based proteomics and concurrent RNAseq analysis, we determine that translation and not transcription of vaccinia virus mRNAs is compromised in cells with deficient RQC activity. Additionally, vaccinia virus infection reduces cellular RQC activity, suggesting that co-option of ZNF598 by vaccinia virus plays a critical role in translational reprogramming that is needed for optimal viral propagation.
2021-04-14 | GSE165732 | GEO