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Chikungunya virus

ABSTRACT: ARUBA CHIKV

PROVIDER: PRJDB8750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR191509_1.fastq.gz	Fastqsanger.gz
	DRR191509_2.fastq.gz	Fastqsanger.gz
	DRR191510_1.fastq.gz	Fastqsanger.gz
	DRR191510_2.fastq.gz	Fastqsanger.gz
	DRR191511_1.fastq.gz	Fastqsanger.gz

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microRNA expression profile in HEK293T cells infected with Chikungunya virus

2014-01-01 | GSE49884 | GEO

Chikungunya Virus Time Course Infection of Human Macrophages

Project description:Human monocyte-derived macrophage cells were infected with Chikungunya virus (CHIKV) to identify and quantify intracellular transcriptional changes that contribute to the host response to infection with CHIKV. RNA was collected from these cells at 8 and 24 hours post-infection (hpi) and were compared to mock-infected cells. The RNAseq data was then analyzed to determine the genes, functions, and signaling pathways that were significantly affected in an effort to predict existing drugs that could be repurposed as potential therapeutics for CHIKV.

2022-03-02 | GSE182287 | GEO

microRNA expression profile in HEK293T cells infected with Chikungunya virus

Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV microRNA expression signature was generated. Cells grown on 6-well plates. Three biological replicates of uninfected and two biological replicates of infected samples

2014-01-01 | E-GEOD-49884 | biostudies-arrayexpress

Gene expression profile in HEK293T cells infected with Chikungunya virus

Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV gene expression signature was generated. Cells grown on 6-well plates. Three biological replicates of uninfected and two biological replicates of infected samples

2014-01-20 | E-GEOD-49985 | biostudies-arrayexpress

Gene expression profile in HEK293T cells infected with Chikungunya virus

2014-01-20 | GSE49985 | GEO

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Project description:Infection with chikungunya virus (CHIKV) causes disruption of draining lymph node (dLN) organization, including paracortical relocalization of B cells, loss of the B cell-T cell border, and lymphocyte depletion that is associated with infiltration of the LN with inflammatory myeloid cells. Here, we find that during the first 24 h of infection, CHIKV RNA accumulates in MARCO-expressing lymphatic endothelial cells (LECs) in both the floor and medullary LN sinuses. The accumulation of viral RNA in the LN was associated with a switch to an antiviral and inflammatory gene expression program across LN stromal cells, and this inflammatory response, including recruitment of myeloid cells to the LN, was accelerated by CHIKV-MARCO interactions. As CHIKV infection progressed, both floor and medullary LECs diminished in number, suggesting further functional impairment of the LN by infection. Consistent with this idea, antigen acquisition by LECs, a key function of LN LECs during infection and immunization, was reduced during pathogenic CHIKV infection.

2024-01-31 | GSE243638 | GEO

Transcriptome analysis of Huh7 cells upon Chikungunya virus infection and capsid transfection reveals regulation of distinct cellular and metabolic pathways

Project description:The purpose of this study is to compare the gene profiles of chikungunya virus (CHIKV) capsid transfected and CHIKV infected Huh7 cells to identify the genes differentially expressed in the presence of the capsid protein during CHIKV infection

2021-03-16 | GSE168910 | GEO

The novel lncRNA ALPHA specifically targets chikungunya virus to control infection

Project description:We set out to determine whether lncRNAs can contribute to additional antiviral immune strategies independently of canonical innate signaling. High-throughput genetic screening of 2200 human lncRNAs led to the identification of the cytoplasmic antiviral lncRNA Antiviral LncRNA Prohibiting Human Alphaviruses (ALPHA) which is transcriptionally induced by alphaviruses and functions independently of IFN to specifically inhibit the replication of CHIKV and its closest relative, O’nyong’nyong virus (ONNV), but not other viruses. Furthermore, we showed that ALPHA interacts with CHIKV genomic RNA and restrains viral RNA replication. Together, our findings reveal that ALPHA and potentially other lncRNAs can mediate non-canonical antiviral immune responses against specific viral pathogens.

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Altered brain pathways following Chikungunya virus infection

Project description:A kinetic analysis of host proteome modifications in the brain of CHIKV-infected mice sampled before and after the onset of clinical symptoms was performed. The combination of 2D-DIGE and iTRAQ proteomic approaches, followed by mass spectrometry protein identification, revealed 177 significantly differentially expressed proteins. This kinetic analysis was characterized by a dramatic down-regulation of proteins prior the appearance of the clinical symptoms followed by an increase expression of a large part of these proteins in the acute phase of symptoms. Bioinformatic analysis of the protein dataset allowed to identify major biological processes altered during the time course of CHIKV infection such as integrin signaling and cytoskeleton dynamics, endosome machinery and receptor recycling related to virus transport and synapse function, regulation of gene expression, and ubiquitin-proteasome pathway. This work gives new information on putative mechanisms that could be associated with severe neurological CHIKV infection-mediated disease. It also describes possible markers or targets that can be used to develop diagnostic and/or antiviral tools.

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