Zika virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA376401 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5309450.fastq.gz | Fastqsanger.gz | |||
| SRR5309451.fastq.gz | Fastqsanger.gz | |||
| SRR5309452.fastq.gz | Fastqsanger.gz | |||
| SRR5309453.fastq.gz | Fastqsanger.gz | |||
| SRR5309454.fastq.gz | Fastqsanger.gz |
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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
Project description:Identifying host factors is key to understanding RNA virus pathogenicity. Besides proteins, RNAs can interact with virus genomes to impact replication. Here, we used proximity ligation sequencing to identify virus-host RNA interactions for four strains of Zika virus (ZIKV) and one strain of dengue virus (DENV-1) in human cells. We found hundreds of coding and non-coding RNAs that bind to DENV and ZIKV viruses. Host RNAs tend to bind to single-stranded regions along the virus genomes and the binding is primarily driven by hybridization energetics. We observed that virus interacting host RNAs tend to be downregulated upon virus infection and identified a conserved set of virus responders that binds to most DENV and ZIKV. Knockdown of several short non-coding RNAs, including miR19a-3p, SCARNA2 and 7SK RNA resulted in a decrease in virus growth, suggesting that they act as virus permissive factors. In addition, the 3’UTR of DYNLT1 mRNA acts as a virus restrictive factor by binding to the conserved dumbbell region on DENV and ZIKV 3’UTR to decrease virus replication. This study demonstrates that host RNAs in themselves can impact virus growth in permissive and restrictive ways, expanding our understanding of host factors and RNA-based gene regulation during virus pathogenesis.
2021-06-10 | GSE176428 | GEO
Project description:Viral interfering RNA (viRNA) has been identified from several viral genomes via directly deep RNA sequencing of the virus-infected cells, including zika virus (ZIKV). Once produced by endoribonuclease Dicer, viRNAs, similar to microRNAs, are loaded onto Argonaute (AGO) family proteins of the RNA-induced silencing complexes (RISCs) to pair with their RNA targets and then initiate cleavage of the target genes. However, identities of functional ZIKV viRNAs and their viral RNA targets remain largely unknown. By combining AGO-associated RNA sequencing, deep sequencing analysis in ZIKV-infected neural stem cells (NSCs), and miRanda target scanning, we have defined 29 ZIKV derived viRNA profiles in NSCs, and established the complex interaction networks between the viRNAs and their viral targets. Our recent study has shown that ZIKV capsid protein interacted with Dicer and antagonized its endoribonuclease activity depending on its histidine (H) at the 41st amino acid. Accordingly, the rescued ZIKV-H41R mutant virus, compared to wild-type ZIKV, no longer suppressed Dicer enzymatic activity and consequently failed to inhibit miRNA biogenesis in NSCs. As a result, much higher levels of viRNAs generated from the ZIKV-H41R virus-infected NSCs, suggesting Dicer-dependent viRNA production. Knockdown of individual RNAi machinery in ZIKV-infected NSCs suggests that viRNA is a limiting factor of ZIKV infection in NSCs. The mapping of viRNAs to their RNA targets is paving a way to further investigate how viRNAs play the role in anti-viral mechanisms or even other unknown biological functions.
2021-02-16 | GSE159916 | GEO
Project description:Zika virus (ZIKV) and dengue virus (DENV) are members of the Flaviviridae family of RNA viruses and cause severe disease in humans. ZIKV and DENV share over 90% of their genome sequences, however the clinical features of Zika and dengue infections are very different reflecting tropism and cellular effects. Here, we used simultaneous RNA sequencing and ribosome footprinting to define the transcriptional and translational dynamics of ZIKV and DENV infection in human neuronal progenitor cells (hNPCs). The gene expression data showed induction of aminoacyl tRNA synthetases (ARS) and the translation-activating PIM1 kinase indicating an increase in RNA translation capacity. The data also reveal activation of different cell stress reponses, with ZIKV triggering a BACH1/2 redox program, and DENV activating the ETF/CHOP endoplasmatic reticulum (ER) stress program. The RNA translation data highlight activation of polyamine metabolism through changes in key enzymes and their regulators. This pathway is needed for eIF5A hypusination and has been implicated viral translation and replication. Concerning the viral RNA genomes, ribosome occupancy readily identifies highly translated open reading frames and a novel upstream ORF (uORF) in the DENV genome. Together, our data highlight both the cellular stress response and also the activation of RNA translation and polyamine metabolism during DENV and ZIKV infection.
2022-07-06 | GSE207347 | GEO
Project description:The recent outbreaks of Zika virus (ZIKV) and its association with birth defects known as Congenital Zika Syndrome warrant investigation on the molecular processes related to its infection and pathogenesis. Among the flavivirus family, only ZIKV is linked to microcephaly as announced by World Health Organization, suggesting uniqueness of ZIKV infection compared to other members. By analyzing the ZIKV-host interactome, we found that the key microRNA (miRNA) processing enzyme Dicer was a leading target of ZIKV capsid protein in neural stem cells (NSCs), and its deficiency facilitated ZIKV infection. Mechanistically, ZIKV capsid can directly interact with Dicer and block its ribonuclease activity, dampening the production of host miRNAs that are essential for neurogenesis. Interestingly, this capsid-mediated immune evasion is specific to ZIKV because capsid proteins from other close flaviviruses, e.g., dengue, yellow fever and West Nile viruses, cannot bind to Dicer or inhibit its function. By molecular mapping, we defined a ZIKV capsid H41R mutant with loss of interaction to Dicer and no longer affecting its activity. More importantly, ZIKV H41R mutant exerted almost no impact on neurogenesis in vitro when expressed in NSCs compared to wild type capsid, and in utero infection of recombinant ZIKV-H41R mutant virus resulted in less inhibition on corticogenesis than wild-type ZIKV in mouse embryos. Interestingly, the epidemic ZIKV strain reinforces the capsid-Dicer interaction by two amino acid substitution compared to ancient Africa strain. Thus, our study demonstrated that capsid-dependent suppression of Dicer function is a unique determinant of ZIKV immune evasion and pathogenesis, which may unveil a new mechanism for ZIKV-mediated microcephaly.
2020-08-04 | GSE137592 | GEO
Project description:miRNA profiles of hUCMSCs infected with ZIKV using Illumina small RNA sequencing platform
2020-05-07 | GSE149983 | GEO
Project description:We repoted the Glioblastoma stem cells(GSCs) infected by two strains of ZIKA virus, the Brazil and Dakar strains. The ZIKV was added into the medium of GSCs for 48 hours, the RNA was harvested after ZIKV infection. We found that the GSCs up-regulated the Type 1&2 interferons after infected by ZIKV
2017-08-23 | GSE102924 | GEO
Project description:The suspected link between infection by Zika virus (ZIKV), a re-emerging flavivirus, and microcephaly, is an urgent global health concern. The direct target cells of ZIKV in developing human fetuses are not clear. Here we show that ZIKV serially passaged in monkey and mosquito cell lines infects human induced pluripotent stem cells (hiPSCs)-derived cortical neural progenitor cells (hNPCs) with much higher efficiency compared to hiPSCs and hNPC-derived immature cortical neurons. Infected hNPCs produces infectious ZIKV particles. Importantly, ZIKV infection increases cell death and dysregulates cell cycle progression, resulted in attenuated hNPC growth. RNA-sequencing analysis of infected hNPCs further reveals transcriptional dysregulation, notably genes in cell cycle pathways. Our results identify human cortical neural precursors as a major and direct target of ZIKV infection and establish a tractable experimental model system to investigate the impact and mechanism of ZIKV on human brain development and a platform to screen therapeutic compounds.
2016-03-04 | GSE78711 | GEO
Project description:Zika virus (ZIKV) is a member of the Flaviviridae family, transmitted by Aedes mosquitoes. ZIKV can be transmitted from pregnant woman to fetus and causes microcephaly and neuronal defects. Patients infected with ZIKV showed increased levels of proinflammatory cytokines compared to healthy individuals and neurological changes even after recovery. However, the detailed mechanism of how neuronal defects occurs after recovery from ZIKV infection has never been investigated in vivo. Here, we found that viral RNA loads were highest in mouse brain tissue 7 days after ZIKV infection and were equivalent to uninfected controls after 21 days, suggesting that mice recovered after 21 days of ZIKV infection. To explore the pathological mechanisms of neuronal defects after recovery from ZIKV infection, we performed RNA-sequencing in mouse cerebral cortex obtained 7 days and 21 days after ZIKV infection.
2024-05-20 | GSE265861 | GEO
Project description:We have generated transgenic Ae. aegypti that express a ZIKV-specific inverted repeat RNA intended to trigger the mosquito siRNA anti-viral immune pathway. To confirm that the transgene is expressed and processed, we performed small RNA sequencing on both Higgs White Eye (HWE) & anti-NS3/4A-ZIKV transgenic Ae. aegypti 24 hours post-bloodmeal
2020-08-26 | GSE156825 | GEO