ZIKV infection increases HUVECs endothelial barrier permeability and activates inflammatory cytokines
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ABSTRACT:
PROVIDER: PRJNA488555 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7768670_1.fastq.gz | Fastqsanger.gz | |||
| SRR7768670_2.fastq.gz | Fastqsanger.gz | |||
| SRR7768668_1.fastq.gz | Fastqsanger.gz | |||
| SRR7768668_2.fastq.gz | Fastqsanger.gz | |||
| SRR7768669_1.fastq.gz | Fastqsanger.gz |
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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
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