Hefer Valley virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA947360 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Crosslinking immunoprecipitation and sequencing was used to characterize nucleocapsid-RNA interactions in Rift Valley fever virus infection. This data set includes illumina HiSeq paired-end reads of Rift Valley fever virus infected HEK293 cells. The sequencing libraries were generated from nucleocapsid-bound RNAs.
2021-10-22 | GSE186067 | GEO
Project description:Rift Valley fever virus causes severe disease in humans and livestock and in some cases can be fatal. There is concern about the use of Rift Valley fever virus as a bioweapon since it can be transmitted through the air, and there are no vaccines or antiviral treatments. Airborne transmission of the virus causes severe inflammation of the brain, yet little is known about the immune response against the virus in this organ. Here, we investigated the immune response in the brain to Rift Valley fever virus following intranasal infection. We determined that microglia, the resident immune cells of the brain, initiate a robust response to Rift Valley fever virus infection and identified a key immune pathway that is critical for the ability of microglia to respond to infection. When this immune pathway is rendered non-functional, mice have a dysregulated response to infection in the brain.
2022-04-27 | GSE200881 | GEO
Project description:Rift Valley Fever Virus genome from Mayotte, Indian Ocean
| PRJNA517473 | ENA
Project description:Rift Valley fever virus Raw sequence reads
| PRJNA518058 | ENA
Project description:Rift Valley fever virus (RVFV) is an important human and livestock pathogen. To better understand the molecular virology and mechanisms of pathogenesis in human HEK293 cells during RVFV MP-12 strain infection, we used high-throughput mRNA sequencing technology to identify and analyze differentially expressed genes and mRNA splicing patterns triggered by infection or by expression of RVFV nucleocapsid protein. Here we supply the results of our RNA-seq analysis of RVFV-infected cells and cells transfected with RVFV nucleocapsid protein expressing plasmids. Some of the results were published in: "Transcriptome profiling in Rift Valley fever virus infected cells reveals modified transcriptional and alternative splicing programs" by Katherine E Havranek, Luke Adam White, Jean-Marc Lanchy, J Stephen Lodmell. PLoS One. 2019 May 28;14(5):e0217497. PMID: 31136639 PMCID: PMC6538246.
2023-09-12 | GSE242551 | GEO
Project description:The Rift Valley Fever (RVF) is an arthropod-borne disease present in several countries of Africa and Middle East. It is caused by RVF virus which can infect both humans and animals. In humans, it leads to various manifestations including hepatitis, encephalitis and death, while in domestic animals it usually causes miscarriage in pregnant females and it is often fatal for the newborn. Not all people or animal infected by the virus present the same disease. Some patients exhibit unapparent or moderate febrile reactions, while others develop severe symptoms. This observation suggests that host genetic factors play a role in controlling the outcome of infection. In this work, we compare the response of two different inbred strains of mice, MBT/Pas and BALB/cByJ, to infection with RVF virus. These strains exhibit different profiles of susceptibility to RVF virus infection. Indeed, MBT/Pas mice rapidly develop high viraemia and die soon after infection, while BALB/cByJ mice have a lower viraemia and die later. Interestingly, mouse embryonic fibroblasts (MEFs) obtained from MBT/Pas foetuses allows higher viral production than BALB/cByJ MEFs. Keywords: expression profiling The experiment was designed to include ARN samples from MBT/Pas and BALB/cByJ MEFs infected with the Rift Valley Fever (RVF) virus, and their respective mock-infected controls; each one of those in triplicate. Therefore, we have used 12 different samples for the study, divided as follows: 3 samples of RVF virus-infected BALB/cByJ MEFs, 3 samples of mock-infected BALB/cByJ MEFs, 3 samples of RVF virus-infected MBT/Pas MEFs and 3 samples of mock-infected MBT/Pas MEFs. Each RNA was extracted from a different culture well.
2010-08-31 | E-GEOD-18064 | biostudies-arrayexpress
Project description:Iso-Seq "full length" transcript sequences were used as one of many guides informing gene model annotation of the Valley Oak genome sequence.
2021-05-22 | GSE174827 | GEO
Project description:The Rift Valley Fever (RVF) is an arthropod-borne disease present in several countries of Africa and Middle East. It is caused by RVF virus which can infect both humans and animals. In humans, it leads to various manifestations including hepatitis, encephalitis and death, while in domestic animals it usually causes miscarriage in pregnant females and it is often fatal for the newborn. Not all people or animal infected by the virus present the same disease. Some patients exhibit unapparent or moderate febrile reactions, while others develop severe symptoms. This observation suggests that host genetic factors play a role in controlling the outcome of infection. In this work, we compare the response of two different inbred strains of mice, MBT/Pas and BALB/cByJ, to infection with RVF virus. These strains exhibit different profiles of susceptibility to RVF virus infection. Indeed, MBT/Pas mice rapidly develop high viraemia and die soon after infection, while BALB/cByJ mice have a lower viraemia and die later. Interestingly, mouse embryonic fibroblasts (MEFs) obtained from MBT/Pas foetuses allows higher viral production than BALB/cByJ MEFs. Keywords: expression profiling
2010-08-31 | GSE18064 | GEO
Project description:Rift Valley fever virus (RVFV) is an encephalitic bunyavirus that can infect neurons in the brain. There are no approved therapeutics that can protect from RVFV encephalitis. Innate immunity, the first line of defense against infection, canonically antagonizes viruses through interferon signaling. We found that interferons did not efficiently protect primary cortical neurons from RVFV, unlike other cell types. To identify alternative neuronal antiviral pathways, we screened innate immune ligands and discovered that the TLR2 ligand Pam3CSK4 inhibited RVFV infection, and other bunyaviruses. Mechanistically, we found that Pam3CSK4 blocks viral fusion, independent of TLR2. In a mouse model of RVFV encephalitis, Pam3CSK4 treatment protected animals from infection and mortality. Overall, Pam3CSK4 is a bunyavirus fusion inhibitor active in primary neurons and the brain, representing a new approach toward the development of treatments for encephalitic bunyavirus infections.
2024-06-18 | GSE241547 | GEO
Project description:WGBS sequencing of Valley Oak bud, catkin and leaf tissues
2021-05-22 | GSE174826 | GEO