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Analysis of Gene Expression in the Recovered Mouse Brain following Zika Virus Infection

ABSTRACT: Analysis of Gene Expression in the Recovered Mouse Brain following Zika Virus Infection

PROVIDER: PRJNA1104568 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28809608_1.fastq.gz	Fastqsanger.gz
	SRR28809608_2.fastq.gz	Fastqsanger.gz
	SRR28809609_1.fastq.gz	Fastqsanger.gz
	SRR28809609_2.fastq.gz	Fastqsanger.gz
	SRR28809610_1.fastq.gz	Fastqsanger.gz

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Analysis of Gene Expression in the Recovered Mouse Brain following Zika Virus Infection

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.

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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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Project description:In this study, we show that CD27+ memory like NK cells generated following Zika virus infection exhibited stem-like features viz., self-renewal pathway, differentiation into effector cells and longer telomeres, and greater therapeutic potential than CD27- and naive CD27+ NK cells when adoptively transferred to Zika virus infected mice. In addition, epigenetic landscape of CD27+ memory like NK is markedly different compared to CD27- NK cells.

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