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ABSTRACT: JEV infected mice brains global transcriptome

PROVIDER: PRJNA1001148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25488389_1.fastq.gz	Fastqsanger.gz
	SRR25488389_2.fastq.gz	Fastqsanger.gz
	SRR25488390_1.fastq.gz	Fastqsanger.gz
	SRR25488390_2.fastq.gz	Fastqsanger.gz
	SRR25488391_1.fastq.gz	Fastqsanger.gz

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Global gene expression profile of Japanese encephalitis virus(JEV) infected cytolytic B16F10 and Non-cytolytic JEV resistant B16F10r

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Single-cell RNA sequencing reveals the landscape of immune cells and the characterization of viral tropism in Japanese encephalitis virus-infected mouse brain

Project description:JEV is a neurotropic pathogen that causes lethal encephalitis in humans. The high susceptibility and massive proliferation of JEV in neurons lead to neuronal damage and dramatical inflammation in central nerves system (CNS). However, the mechanisms by which JEV preferentially infects neurons and induces massive neuroinflammation are largely unknown. Here, we found that JEV mainly distributed in cerebral cortex, striatum and thalamus in brain of infected mice, indicating the tissue or cell type bias. Cells in these regions of JEV-infected mice showing different symptoms (mild, moderate and severe) were isolated and subjected to scRNA-seq. 88000 single cells were obtained based on top differentially expressed genes, and 34 clusters and 10 major cell types were identified. As demonstrated by scRNA-seq and flow-cytometry assay, activated microglia cells and infiltrating immune cells including monocyte & macrophage, T cells and NK cells which are responsible for inflammatory response were increased in JEV-infected brain in a symptom severity-dependent manner. Furthermore, the subclusters of these cells and the cell-cell interaction network were analyzed. More communications between individual cells and significant increase in ligand receptor pairs associated with tight junctions, chemokines and antigen-presenting molecules were shown in JEV-infected mouse brain, suggesting upregulation of cellular permeability, inflammation and antiviral response. To identify which subtype(s) of neurons is/are targeted by JEV, 27874 neuronal cells were reclustered to 15 subsets. By analyzing the correlation between the expression of JEV E gene and neuronal genes, we found that Baiap2high neurons are highly permissive to JEV.

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Project description:Japanese encephalitis virus (JEV) is the leading cause of epidemic encephalitis worldwide. JEV-induced neuroinflammation is characterized by profound neuronal cells damage accompanied by activation of glial cells. Albeit long non-coding RNAs (lncRNAs) have been emerged as important regulatory RNAs with profound effects on various biological processes, it is unknown how lncRNAs regulate JEV-induced inflammation. Here, using microarray approach, we identified 618 lncRNAs and 1007 mRNAs differentially expressed in JEV-infected mice brain.

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Global gene expression profile of Japanese encephalitis virus(JEV) infected cytolytic B16F10 and Non-cytolytic JEV resistant B16F10r

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Project description:Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus and causes acute encephalitis with high mortality rate in humans. Despite the demonstration of difference in neuroinvasiveness between JEV strains, little is known about host gene response upon infection of virulent and attenuated JEV strains. To understand the pathogenesis mechanism of JEV infection, we performed a comparative genome-wide microarray analysis (Affymetrix, mouse genome 430 2.0 with 45101 probe sets) of genes expressed in the mice brains three days post intracerebrally inoculated with JEV strains of different neurovirulence. We found that the virulent strain of JEV (RP-9) tended to affect the host gene expression more profoundly than the attenuated one (RP-2ms), as 961 vs. 665 and 655 vs. 509 genes were at least two-fold upregulated and downregulated by RP-9 and RP-2ms, respectively. In order to understand the host defense response against JEV, we further analyzed the microarray data with special focus on immune response. The expression levels of selected genes were further verified by quantitative RT-PCR at 1-, 3- and 5-day post JEV infection. The differentially regulated genes reported here likely contribute to the neurovirulent phenotype by modulating the host immunity, viral replication and/or cytotoxicity. Keywords: day3, virus (1 x 10^4 PFU), intracerebrally (ic) inoculated, brain total RNA

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Project description:Differentially expressed miRNA upon JEV infection in the mice brains

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Project description:Japanese Encephalitis Virus (JEV) modulates different proteins at different time points of infection to favour its propagation in the host cells. The dysregulation of intertwined pathways in the host has implications for virus pathogenesis. This study aims to decipher the global proteome of Japanese encephalitis infected THP-1 derived macrophages at 24 hours post-infection and 48 hours post-infection, which will further help to deduce the interwoven pathways regulated upon JEV infection.

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