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ZIKV RNA Structure

ABSTRACT: Integrative analysis of Zika virus genome RNA structure reveals critical determinants of viral infectivity

PROVIDER: PRJEB28648 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2795070.fastq.gz	Fastqsanger.gz
	ERR2795080.fastq.gz	Fastqsanger.gz
	ERR2795071.fastq.gz	Fastqsanger.gz
	ERR2795081.fastq.gz	Fastqsanger.gz
	ERR2795072.fastq.gz	Fastqsanger.gz

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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.

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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

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Project description:The full transcriptional RIPK3-dependent transcriptional potential is unknown. Here, we found that RIPK3 is a dominant driver of anti-viral transcription in neurons following Zika virus infection.

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Assessing the role of RHIM proteins in ZIKV-induced inflammatory transcription in neurons

Project description:We previously have found that RIPK3 induces robust anti-viral and inflammatory transcriptional signaling in death-resistant MEFs in a RIPK1-and TRIF-dependent manner. We nexted wanted to assess whether this mechanism was conserved in neurons during Zika virus infection.

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Next Generation Sequencing Facilitates Quantitative Analysis of Mock/ZIKV infected Guinea Pig Lung Transcriptomes

Project description:Whether Zika virus (ZIKV) could be transmitted via aerosol routes remains unknown. In this study, we demonstrated that aerosolized ZIKV is fully infectious in vitro and in vivo.Transcriptome analysis further revealed that genes expression related to viral process, biological regulation and immune system response were significantly changed.

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ZIKV and DENV-2 sfRNA RNA Pull down Hela extract LC-MSMS

Project description:Insect-borne flaviviruses produce a 300-500 base long noncoding RNA, termed sfRNA, by stalling the cellular 5’-3’ exoribonuclease XRN1 via structures located in their 3’ untranslated regions. In this study we demonstrate that the production of sfRNAs by Zika virus results in the repression of XRN1 similar to what we have previously shown for other flaviviruses. Using protein-RNA reconstitution and a stringent RNA pulldown assay, we demonstrate that the sfRNA from both dengue type 2 and Zika viruses interact with a common set of 21 RNA binding proteins that influence post-transcriptional processes in the cell, including splicing, RNA stability and translation. We demonstrate that four of these interacting proteins - DDX6 and EDC3 (RNA decay factors), PHAX1 (a regulator of the biogenesis of the splicing machinery) and APOBEC3C (a nucleic acid editing deaminase) are inherently antiviral restriction factors for Zika virus infection. Furthermore, we demonstrate that cellular mRNA decay regulation as well as cellular RNA splicing are compromised during Zika virus infection. Collectively, these data demonstrate the large extent in which Zika virus sfRNAs interact with cellular RNA binding proteins as well as the potential for widespread dysregulation of post-transcriptional control which likely limits the effective response of the cell to viral infection.

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Project description:Zika virus (ZIKV) is an emerging, mosquito-borne pathogen associated with a widespread 2015–2016 epidemic in the Western Hemisphere and a proven cause of microcephaly and other fetal brain defects in infants born to infected mothers. ZIKV infections have been also linked to other neurological illnesses in infected adults and children, including Guillain-Barré syndrome (GBS), acute flaccid paralysis (AFP) and meningoencephalitis, but the viral pathophysiology behind those conditions remains poorly understood. Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We perform RNA seq, and global trancriptome analysis to corroborate the effect of retinoic acid in SH-SY5Y cells. Then we analyze the virus infection in differentiated and undifferntiated cells. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation. Enhanced ZIKV infectivity in a neural cell line following differentiation may contribute to viral neuropathogenesis in the developing or mature central nervous system.

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