Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Correlative gene expression to protective seroconversion in Rift Valley Fever vaccinates

ABSTRACT: 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.

ORGANISM(S): Bos taurus

PROVIDER: GSE71417 | GEO | 2016/09/16

SECONDARY ACCESSION(S): PRJNA291193

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effects of Rift Valley fever virus infection on gene expression and alternative splicing in HEK 293 cells

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

Alteration in the Culex pipiens transcriptome reveals the implication of the mosquito immune system during Rift Valley fever phlebovirus infection

Project description:Rift valley fever (RVF) is an emerging zoonotic disease and it is caused by Rift valley fever phlebovirus (RVFV). This virus is commonly transmitted in endemic areas between wild ruminants and mosquitoes, mainly by mosquitoes of Culex and Aedes genus. Starting from 2000, several outbreaks have been reported outside the African continent, in countries facing the Mediterranean Sea, such as Saudi Arabia. The available vaccines for ruminants present limited efficacy or residual pathogenic effects. Consequently, new strategies are urgently required to limit the expansion of this zoonotic virus. The main objective of this work is to investigate the molecular responses of Culex pipiens to RVFV focusing mainly on genes implicated in the classical innate immunity pathways, RNAi mechanism and apoptosis process in order to elucidate the implicated genes in viral infection. The immune altered genes here described could be potential targets to control RVFV infection in mosquitoes. Some of the genes related to the immune defense response were previously described in others mosquito-arbovirus models, as also in Drosophila and human. To our knowledge, this study elucidates for the first time the Cx. pipiens-RVFV interaction in terms of defense infection-response, which was largely under studied and provides information to develop new approaches to prevent and control the expansion of the virus in the future.

2020-11-02 | GSE142339 | GEO

MAVS mediates a protective immune response in the brain to Rift Valley fever virus

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

Temporal alterations in the HSAEC transcriptome following infection by virulent and attenuated strains of Rift Valley Fever Virus

Project description:Rift Valley fever virus (RVFV) causes major outbreaks among livestock, characterized by “abortion storms” in which spontaneous abortion occurs in almost 100% of pregnant ruminants. Humans can also become infected with mild symptoms that can progress to more severe symptoms, such as hepatitis, encephalitis, and hemorrhagic fever. The goal of this study was to use RNA-sequencing (RNA-seq) to analyze the host transcriptome in response to RVFV infection. G2/M DNA damage checkpoint, ATM signaling, mitochondrial dysfunction, regulation of the antiviral response, and integrin-linked kinase (ILK) signaling were among the top altered canonical pathways with both the attenuated MP12 strain and the fully virulent ZH548 strain. Although several mRNA transcripts were highly upregulated, an increase at the protein level was not observed for the selected genes, which was at least partially due to the NSs dependent block in mRNA export. Inhibition of ILK signaling, which is involved in cell motility and cytoskeletal reorganization, resulted in reduced RVFV replication, indicating that this pathway is important for viral replication. Overall, this is the first global transcriptomic analysis of the human host response following RVFV infection, which could give insight into novel host responses that have not yet been explored.

2017-08-11 | GSE102481 | GEO

Characterization of nucleocapsid-RNA interactions in Rift Valley fever virus infected cells

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

MAVS mediates a protective immune response in the brain to Rift Valley fever virus

Project description:MAVS mediates a protective immune response in the brain to Rift Valley fever virus

| PRJNA827135 | ENA

Comparison of MBT/Pas and BALB/cByJ MEFs response after infection with Rift Valley Fever virus

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:Genetic diversity of recombinant Rift Valley fever virus MP-12 strain infectious clones derived from Vero cells

| PRJNA674398 | ENA

Non-protective immune imprint underlies failure of S. aureus IsdB vaccine

Project description:The failure to date of all S. aureus vaccine trials has been a conundrum and underlines fundamental flaws in current translational models. A major difference between humans and laboratory animals is the early and frequent exposure of humans to S. aureus compared to animals, which is not accounted for in vaccine studies. In recapitulating the failed IsdB human vaccine trial, we showed that mice previously infected with S. aureus do not mount a protective vaccine antibody response, unlike naïve mice. S. aureus infection induces robust but non-neutralizing anti-IsdB antibodies that target different but overlapping IsdB epitopes compared to IsdB vaccine. In the setting of prior S. aureus infection, however, IsdB vaccine recalls the non-protective humoral response which further competes and reduces efficacy of protective vaccine-generated specific antibodies. Vaccination against the heme-binding domain of IsdB or select IsdB epitope can overcome interference by S. aureus infection. Using an adoptive transfer model, we showed that human serum antibodies against IsdB and another vaccine target, ClfA, are also non-protective and blocked anti-staphylococcal immunity conferred by passive immunizations. Overall, our study demonstrates proof of concept that failure of anti-S. aureus active and passive immunizations could be explained by non-protective imprint of prior host-pathogen interaction.

2023-01-28 | GSE193543 | GEO