Ontology highlight
ABSTRACT:
PROVIDER: PRJNA825509 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18713868_1.fastq.gz | Fastqsanger.gz | |||
| SRR18713868_2.fastq.gz | Fastqsanger.gz | |||
| SRR18713869_1.fastq.gz | Fastqsanger.gz | |||
| SRR18713869_2.fastq.gz | Fastqsanger.gz | |||
| SRR18713870_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:Rift Valley Fever Virus (RVFV), a negative-stranded RNA virus, is the etiological agent of the vector-borne zoonotic disease, Rift Valley Fever (RVF). In both humans and livestock, protective immunity can be achieved through vaccination. Earlier and more recent vaccine trials in cattle and sheep demonstrated a strong neutralizing antibody and total IgG response induced by the RVFV vaccine, MP-12. From previous work, protective immunity in sheep and cattle vaccinates normally occurs from 7 to 21 days after inoculation with MP-12. While the serology and protective response induced by MP-12 has been studied, little attention has been paid to the underlying molecular and genetic events occurring prior to the serologic immune response. To address this, we isolated RNA from whole blood from vaccinates over a time course of 21 days before and after inoculation during a recent vaccine trial with MP-12. This RNA time course was deeply sequenced by RNASeq and bioinformatically analyzed. Our results revealed time-dependent activation or repression of numerous gene ontologies and pathways related to immune response and regulation. Additional analyses identified a correlative relationship between specific genes related to immune activity and protective immunity prior to serologic detection of antibody response. These data provide an important proof of concept for identifying molecular and genetic components underlying the immune response to vaccination and protection prior to serologic detection.
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Project description:Mathematical model for Rift Valley Fever transmission between cattle and mosquitoes without infectious eggs.
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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.
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