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Metformin restrains ZIKV replication and alleviates virus-induced inflammatory responses in microglia

ABSTRACT: Metformin restrains ZIKV replication and alleviates virus-induced inflammatory responses in microglia

PROVIDER: PRJNA962999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24348960_1.fastq.gz	Fastqsanger.gz
	SRR24348960_2.fastq.gz	Fastqsanger.gz
	SRR24348961_1.fastq.gz	Fastqsanger.gz
	SRR24348961_2.fastq.gz	Fastqsanger.gz
	SRR24348962_1.fastq.gz	Fastqsanger.gz

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Metformin restrains ZIKV replication and alleviates virus-induced inflammatory responses in microglia

Project description:C20 were pre-treated with metformin at specified concentration (5 mM) for 2 h, followed by ZIKV infection at MOI 3. After infection of 1.5 h, cells were washed three times with PBS. Medium containing metformin was again supplemented and maintained during the culture. The total RNA of samples at 16 and 48 h were extracted for RNA-seq analysis. We then performed differential expression analysis using data obtained by RNA-seq of ZIKV infection and metformin treatment (16 h and 48 h).

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Project description:To determine the effect of Zika virus infection on pre-implantation embryonic development, we performed single blastocyst RNA-Seq on MOCK and ZIKV infected embryos. ZIKV infection results in an increased risk of spontaneous abortion and poor intrauterine growth although the mechanisms underlying fetal loss remain undetermined. Little is known about the impact of ZIKV infection during the earliest stages of pregnancy, or pre- and peri-implantation, because most current studies of ZIKV infection in pregnancy models focus on post-implantation stages. Here, we demonstrate that trophectoderm cells of pre-implantation human and mouse embryos can be efficiently infected with ZIKV, and that trophectoderm can propagate virus causing cell death of neural progenitors. These findings were corroborated by our demonstration that hESC-derived trophectoderm cells are infected by ZIKV in a dose dependent manner. RNAseq of single blastocysts revealed key transcriptional changes in cellular and physiologic functions upon ZIKV infection, including nervous system development and function, prior to commitment to the neural cell lineage. Finally, the pregnancy rate of mice infected pre-implantation was > 50% lower than females infected at E4.5. These results demonstrate that pre-implantation ZIKV infection of trophectoderm leads to miscarriage or spontaneous abortion. Moreover, pre- and peri-implantation ZIKV infects trophectoderm cells that propagate virus over time causing cell death in neural progenitors. Cumulatively, these data demonstrate that vertical pre- and peri-implantation ZIKV infection of trophectoderm impairs fetal development and causes neural progenitor cell death, elucidating a previously unappreciated association of pre- and peri-implantation ZIKV infection and microcephaly.

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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) 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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