Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of CD8+ T cells in immune-privileged organs of ZIKV-infected Ifnar1-/- mice

ABSTRACT: Zika virus (ZIKV) infection caused neurological complications and male infertility, leading to the accumulation of antigen-specific immune cells in immune-privileged organs (IPOs). Thus, it is important to understand the immunological responses to ZIKV in IPOs. We extensively investigated the ZIKV-specific T-cell immunity in IPOs in Ifnar1-/- mice, based on an immunodominant epitope E294-302 tetramer. The distinct kinetics and functions of virus-specific CD8+ T cell infiltrated into different IPOs were characterized. The E294-302-specific TCRαβs are featured within the IPOs in different infection phases with the majority of clonotypes utilizing TRAV9N-3 paired with diverse TRBV chains. Specific chemokine receptors, Ccr2 and Ccr5, were selectively expressed in the E294-302-specific CD8+ T cells within the brain and testicle, indicating an IPO-orientated migration of virus-specific T cells after infection. Overall, this study adds to the understanding of virus-specific CD8+ T cell responses for controlling and clearing ZIKV infection in IPOs.

ORGANISM(S): Mus musculus

PROVIDER: GSE229856 | GEO | 2023/12/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Molecular Signatures Associated with ZIKV Exposure in Human Cortical Neural Progenitors and Astrocytes

Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) and astrocytes exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Upon ZIKV infection, astrocytes exhibit more prominent transcriptome changes than hNPCs, particularly enriching genes related to inflammatory response and cytokine production pathways. Our analyses reveal cell-type- and strain-specific molecular signatures associated with ZIKV infection, and identify astrocytes as a major direct target of ZIKV. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients. Gene Expression Analyses of the cells infected with different flaviviruses

2016-08-23 | E-GEOD-80434 | biostudies-arrayexpress

RNA sequencing of Aedes mosquitoes infected with Zika virus (ZIKV) or Dengue virus (DENV)

Project description:Zika virus (ZIKV), a pathogen of global health concern, is transmitted to humans by Aedes mosquitoes. However, the molecular interactions between the vector and the virus remain largely unexplored. We demonstrated that ZIKV and dengue virus (DENV) have similar tropism and infection kinetics in two mosquito strains with different degrees of susceptibility to infection. Comparison of Aedes aegypti’s molecular responses to ZIKV and DENV infection indicated that around 40% of the mosquito’s infection-responsive transcriptome is virus-specific. Regulated genes also included key factors of the mosquito’s anti-viral immunity, pointing to the possible involvement of the Toll innate immune pathway. Comparison of ZIKV and DENV infection-responsive transcriptome data to those for yellow fever virus and West Nile virus identified 26 genes likely to play key roles in virus infection of Aedes mosquitoes. Through reverse genetic analyses, we showed that the Toll and the Jak/Stat innate immune pathways mediate increased resistance to ZIKV infection, and the virus use vATPase and inosine-5’-monophosphate dehydrogenase as mosquito’s host factors.

2017-11-07 | GSE96605 | GEO

Molecular Signatures Associated with ZIKV Exposure in Human Cortical Neural Progenitors

Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients.

2016-08-23 | GSE80434 | GEO

ZIKV prevents host mRNA export from the nucleus by disrupting UPF1 function

Project description:Zika virus (ZIKV) is a mosquito-borne virus that can have dramatic neurodevelopmental consequences when infection occurs in utero. Previous studies demonstrated that ZIKV downregulates the master regulator of nonsense mediated decay, UPF1. To examine whether this process contributes to disruption of neural development, we investigated the effect of ZIKV infection on UPF1 interaction with host RNA in neural progenitor cells. Here, we show that ZIKV-mediated disruption of UPF1 function in neural progenitor cells causes retention of mRNA in the nucleus, resulting in decreased protein levels of specific transcripts involved in neural differentiation.

2022-12-22 | GSE160201 | GEO

Effects of Zika virus infection on the metabolome of pregnant women: a longitudinal study

Project description:Zika virus (ZIKV) is a mosquito-borne +ssRNA virus that can cause abnormal development in human fetal central neuron system and even lead to stillbirth. Despite the popularity of studies in this area recently, there is currently still no sufficient treatment for it. Knowledge on how ZIKV infection impact human metabolisms is still lacking. Untargeted metabolomics can profile the overall change in metabolites after infection, thus provide hypothesis for specific investigations. We here performed a Nuclear Magnetic Resonance spectroscopy (NMR)-based untargeted case-control metabolomics study on urine of ZIKV-infected pregnant women. We collected samples monthly from the first trimester till up to 6 months of ZIKV-infected and non-infected individuals and modelled the longitudinal data. We identified 3-aminoisobutyrate and trigonelline with significantly higher levels in the ZIKV-infected patients, while 11 metabolites (fucose, 2-hydroxyglutarate, N-acetyl-glutamine, dimethylamine, 4-hydroxyphenethyl alcohol, creatinine, lactate, threonine, histidine, pseudouridine, and 1-methylnicotinamide) had significantly lower levels. We also identified 2 metabolites, including glucose and 1-methylnicotinamide, where the trends over time of the intensity levels between the two groups were significantly different. These metabolites suggested further study on tryptophan, NAD+, pyrimidine, and glucose metabolisms. These metabolomic changes may lead us to a better understanding of mechanisms that cause poor fetal outcomes as well as effects of virus infection on human pregnancy.

2022-01-03 | ST002048 | MetabolomicsWorkbench

Inter and intra-lineage genetic diversity of Zika virus differs for American isolates

Project description:Zika virus (ZIKV) is a mosquito-transmitted positive-sense RNA virus in the family Flaviviridae. ZIKV infections are associated with neurodevelopmental deficiencies termed Congenital Zika Syndrome. ZIKV strains are grouped into three phylogenetic lineages: East African, West African, and Asian, which contains the American lineage. RNA virus genomes exist as genetically-related sequences. The heterogeneity of these viral populations is implicated in viral fitness, and genome diversity is correlated to virulence. This study examines genetic diversity of representative ZIKV strains from all lineages utilizing next generation sequencing (NGS). Inter-lineage diversity results indicate that ZIKV lineages differ broadly from each other; however, intra-lineage comparisons of American ZIKV strains isolated from human serum or placenta show differences in diversity when compared to ZIKVs from Asia and West Africa. This study describes the first comprehensive NGS analysis of all ZIKV lineages and posits that sub-consensus-level diversity may provide a framework for understanding ZIKV fitness during infection.

2018-12-31 | E-MTAB-5945 | biostudies-arrayexpress

Male Germ Cells Support Long-Term Propagation of Zika Virus

Project description:Evidence of male-to-female sexual transmission of Zika virus (ZIKV) and viral RNA in semen and sperm months after infection support a potential role for testicular cells in ZIKV propagation. Here, we demonstrate that germ cells (GC) are most susceptible to ZIKV. We find that only GC infected by ZIKV, but not those infected by dengue fever (DENV) and yellow fever virus (YFV), produce high levels of infectious virus. This observation coincides with decreased expression of interferon-stimulated gene Ifi44l in ZIKV-infected GC and over-expression of Ifi44l results in reduced ZIKV production. Using primary human testicular tissue, we demonstrate that human GC are also permissive for ZIKV infection and production. Finally, we identify berberine chloride as a potent inhibitor of ZIKV infection in both murine and human testes. Together, these studies identify a potential cellular source for propagation of ZIKV in testes and a candidate drug for preventing sexual transmission of ZIKV.

2018-06-06 | GSE113177 | GEO

Host and genetic viral adaptations enable development of an immunocompetent mouse model of Zika virus infection

Project description:Host and genetic viral adaptations enable development of an immunocompetent mouse model of Zika virus infection. This study explored the effect of wildtype Zika virus (ZIKV) and mouse adapted ZIKV infection on the transcriptional profile of mouse adult neuronal stem cells.

2018-04-05 | GSE112711 | GEO

Zika virus infection reprograms global transcription of host cells to allow sustained infection

Project description:Zika virus (ZIKV) is an emerging virus causally linked to neurological disorders, including congenital microcephaly and Guillain–Barré syndrome. There are currently no targeted therapies for ZIKV infection. To identify novel antiviral targets and to elucidate the mechanisms by which ZIKV exploits the host cell machinery to support sustained replication, we analyzed the transcriptomic landscape of human microglia, fibroblast, embryonic kidney, and monocyte-derived macrophage cell lines before and after ZIKV infection.

2017-03-01 | GSE93870 | GEO

Transcriptional changes during naturally-acquired ZIKA Virus infection render dendritic cells highly conducive to viral replication

Project description:Although dendritic cells (DCs) are among the human cell population best equipped for cell-intrinsic antiviral immune defense, they seem highly susceptible to infection with Zika Virus (ZIKV). Using highly-purified mDC isolated from individuals with naturally-acquired acute infection, we here show that ZIKV induces profound perturbations of transcriptional signatures relative to uninfected patients. Interestingly, we noted a remarkable downregulation of antiviral Interferon-stimulated genes and innate immune sensors, suggesting that ZIKV can actively suppress Interferon-dependent immune responses. In contrast, several host factors known to support ZIKV infection were strongly upregulated during natural ZIKV infection; these transcripts included AXL, the main entry receptor for ZIKV, SOCS3, a negative regulator of ISG expression, and IDO-1, a recognized inducer of regulatory T cell responses. Thus, during in vivo infection, ZIKV can transform the transcriptome of dendritic cells in favor of the virus to render these cells highly conducive to ZIKV infection.

2017-12-18 | GSE101878 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data