Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Zika virus

ABSTRACT: Transposon mutagenesis of the Zika virus genome highlights regions essential for RNA replication and restricted for immune evasion

PROVIDER: PRJNA358012 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5119960.fastq.gz	Fastqsanger.gz
	SRR5119970.fastq.gz	Fastqsanger.gz
	SRR5119961.fastq.gz	Fastqsanger.gz
	SRR5119962.fastq.gz	Fastqsanger.gz
	SRR5119963.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

Prolyl hydroxylation is required for maturation and secretion of Zika virus non-structural protein 1

Project description:Mosquito-borne flaviviruses such as Zika virus (ZIKV) and dengue virus (DENV) have a high epidemic potential and are associated with a wide range of possible outcomes, from asymptomatic infections to severe complications. The flavivirus non-structural protein 1 (NS1), which can be membrane-bound as well as secreted from the cell, plays important roles in viral replication, immune evasion and pathogenesis. To identify the interactome of ZIKV NS1, we infected Huh7 and neural progenitor cells with recombinant ZIKV encoding a FLAG-tagged NS1 and analysed the binding partners with quantitative mass spectrometry. In both cell types, multiple prolyl hydroxylase enzymes were identified as NS1 interactors and mass spectrometry data showed that NS1 contains potential hydroxyproline residues at positions 181, 267 and 281, indicating that these enzymes are involved in post-translational modification of NS1. Chemical inhibition of prolyl hydroxylase enzymes reduced ZIKV RNA levels and titers, as well as NS1 glycosylation, plasma membrane localization and secretion. Mutagenesis of the proline residue at position 281 moderately impaired proper expression of NS1, although viral replication was unaffected. In contrast, substituting proline at position 267 strongly dysregulated NS1 expression and reversions to the wild-type sequence were observed already after passage 1, suggesting that this mutation leads to severe replication defects. Our results identify prolyl hydroxylation as an essential post-translational modification of ZIKV NS1.

2025-01-28 | PXD041488 | Pride

Microarray analysis of MRC-5 cells infected with Zika virus strains

Project description:To better understand the critical drivers of Zika virus pathogenicity, we used microarray analysis to evaluate the host responses triggered by Zika virus infection in MRC-5 cells.

2021-03-23 | E-MTAB-10292 | biostudies-arrayexpress

RNA-seq transcript and gene data on zika exposed and zika naïve samples

Project description:RNA-seq count data at 3 timepoints was generated for Zika-exposed and Zika-naïve individuals in order to assess associated signatures

2019-04-17 | GSE129882 | GEO

Zika genome

Project description:Zika genome

| PRJEB34688 | ENA

Genome organization of dengue and Zika viruses

Project description:Dengue and Zika are closely related members of the Flaviviridae family of positive, single-stranded RNA viruses and are of global clinical importance. These viruses utilize an 11kb RNA genome for translation and replication, and much remains to be learnt about how the entire genome folds to enable virus function. Here, we performed high throughput RNA secondary structure and pair-wise interaction mapping on four dengue serotypes and four Zika strains within their virus particles. We identified structures that are associated with translation pausing, and are evolutionary conserved by integrating synonymous mutation rates into our analysis. Genome-wide interaction mapping revealed alternative structures, as well as extensive long-range RNA interactions – including the known circularization signals– within the virus particles. Many of these long-range interactions are conserved across the viruses and/or clustered into “hubs” that are shown to be functionally important. This comprehensive structural resource of dengue and Zika viruses reveals that viral genome organization is much more complex than previously appreciated and deepens our understanding of the molecular basis for viral pathogenesis.

2019-02-28 | GSE106483 | GEO

Transcriptomics in Zika virus-infected human brain organoids

Project description:PolyA+ RNA sequencing of Zika virus-infected human brain organoids at 5 days post-infection.

2017-04-03 | E-MTAB-4811 | biostudies-arrayexpress

CRISPR screen for the identification of host factors for ZIKA virus infection

Project description:To search for host factors regulating Zika virus infection, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of enrichment of their mutant clones within a pooled loss-of-function library upon Zika virus infection.

2023-05-31 | E-MTAB-11945 | biostudies-arrayexpress

Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (Ribo-Seq)

Project description:Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that causes severe outbreaks in human populations. ZIKV infection leads to the accumulation of small non-coding viral RNAs (known as sfRNAs) that are crucial for evasion of antiviral responses and for viral pathogenesis. However, the mechanistic understanding of how sfRNAs function remains incomplete. Here, we use recombinant ZIKVs and ribosome profiling of infected human cells to show that sfRNAs block translation of antiviral genes. Mechanistically, we demonstrate that specific RNA structures present in sfRNAs trigger PKR activation, which instead of limiting viral replication, enhances viral particle production. Although ZIKV infection induces mRNA expression of antiviral genes, translation efficiency of type I interferon and interferon stimulated genes were significantly downregulated by PKR activation. Our results reveal a novel viral adaptation mechanism mediated by sfRNAs, where ZIKV increases its fitness by repurposing the antiviral role of PKR into a proviral factor.

2024-04-28 | GSE254253 | GEO

Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (RNA-Seq)

2024-04-28 | GSE254252 | GEO

zika

Project description:nghien cuu ve virut zika

| PRJEB13387 | ENA