Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The novel lncRNA ALPHA specifically targets chikungunya virus to control infection

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184306 | GEO | 2022/09/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MAVS signaling is required for preventing persistent chikungunya heart infection and chronic vascular tissue inflammation

Project description:Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations. However, how CHIKV infection leads to heart disease remains unknown. Here, using C57BL/6 mice we show that cardiac fibroblasts are the main target of CHIKV infection in the heart, and that cardiac tissue infection induces activation of the type I interferon (IFN-I) pathway in both infected and non-infected cardiac cells. The loss of IFN-I signaling results in increased CHIKV infection, virus spreading, and apoptosis in cardiac tissue. Importantly, signaling through the mitochondrial antiviral-signaling protein (MAVS) is essential for efficient CHIKV clearance from the heart. Indeed, persistent infection in cardiac tissue of MAVS-deficient mice leads to cardiac damage characterized by focal myocarditis and major vessel vasculitis. This study provides mechanistic insight on how CHIKV can lead to cardiac damage, underscoring the importance of monitoring cardiac function in patients with CHIKV infections.

2023-06-10 | GSE204689 | GEO

Chikungunya virus

Project description:ARUBA CHIKV

| PRJDB8750 | ENA

Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO

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

Transcription profiling by array of Vero cells infected by different Chikungunya virus strains to identify common human host genes involved in pathogenesis of different Chikungunya viruses

Project description:In this study, we aim to identify common host genes involved in pathogenesis of different Chikungunya virus strains as an attempt to recognize probable antiviral targets. We have compared the host gene regulation after infection of monkey kidney cell line (Vero) with two different wild type CHIKV strains i.e. S 27 (human, ECSA), and DRDE-06 (human, ECSA). Vero cells were mock infected or infected with two Chikungunya virus strains (S 27 and DRDE-06) and harvested at 8hpi and 18hpi. The total RNA was extracted and microarray was done using Agilent protocol.

2021-10-28 | E-MTAB-6645 | biostudies-arrayexpress

Insect-Specific Chimeric Viruses Potentiated Antiviral Responses and Inhibited Pathogenic Alphavirus Growth in Mosquito Cells

Project description:Most alphaviruses are transmitted by mosquito vectors and infect a wide range of vertebrate hosts, with a few exceptions. Eilat virus (EILV) in this genus is characterized by a host range restricted to mosquitoes. Its chimeric viruses have been developed as safe and effective vaccine candidates and diagnostic tools. Here, we investigated the interactions between these insect-specific viruses (ISVs) and mosquito cells, unveiling their potential roles in determining vector competence and arbovirus transmission. By RNA sequencing, we found that these ISVs profoundly modified host cell gene expression profiles. Two EILV-based chimeras, consisting of EILV’s nonstructural genes and the structural genes of Chikungunya virus (CHIKV) or Venezuelan equine encephalitis virus (VEEV), namely EILV/CHIKV (E/C) and EILV/VEEV (E/V), induced more intensive transcriptome regulation than parental EILV and activated different antiviral mechanisms in host cells. We demonstrated that E/C robustly promoted antimicrobial peptide production and E/V strongly upregulated the RNA interference pathway components. This also highlighted the intrinsic divergences between CHIKV and VEEV, representatives of the Old World and New World alphaviruses. In contrast, EILV triggered a limited antiviral response. We further showed that initial chimera infections efficiently inhibited subsequent pathogenic alphavirus replication, especially in the case of E/V infection, which almost prevented VEEV and Sindbis virus (SINV) superinfections. Altogether our study provided valuable information on developing ISVs as biological control agents.

2023-01-19 | GSE220562 | GEO

A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

Project description:The emerging alphavirus chikungunya virus (CHIKV) has infected millions of people. However, the factors modulating disease outcome remain poorly understood. We show that depletion of the gut microbiota in oral antibiotic-treated or germ-free mice leads to greater CHIKV infection and spread within one day of virus inoculation. Perturbation of the gut microbiota alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interferon (IFN). Consequently, circulating monocytes express fewer IFN-stimulated genes and become permissive for CHIKV infection. Reconstitution with a single commensal bacterial species, Clostridium scindens, or its derived metabolite, the bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restrict systemic CHIKV infection and transmission back to vector mosquitoes. Thus, commensal gut bacteria modulate antiviral immunity and levels of circulating alphaviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects virus dissemination and potentially, epidemic spread

2020-05-13 | GSE150387 | GEO

A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

2020-06-09 | GSE152043 | GEO

Pathogenesis of chikungunya virus infection associated with fatal outcome

Project description:Chikungunya virus (CHIKV) is a mosquito-borne virus that causes acute, subacute, and chronic human diseases and can cause neurological complications and death. Here, we combined epidemiological, virological, histopathological, cytokine, molecular dynamics, metabolomics, proteomics, and genomic analyses to investigate viral and pathophysiologic factors that contribute to deaths caused by chikungunya (CHIK). Our results indicate that CHIK-deaths presented multiple organs infection, central nervous system damage, and exhibited significantly elevated serum levels of pro-inflammatory cytokines and chemokines compared to survivors. The histopathology, metabolite, and proteomic signatures of CHIK-deaths revealed hemodynamic disorders and dysregulated immune system response. CHIKV East-Central-South-African lineage caused fatal and survivor cases, and CHIKV crosses the blood–brain barrier without tight junction alterations. IFN-λ3 was highly expressed in fatal cases but did not present a direct antiviral effect on CHIKV replication in vitro. In summary, our results reveal insights to improve understanding of CHIK pathogenesis, especially the pathophysiology of fatal infections.

2024-06-16 | PXD043815 | Pride

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.

2015-07-07 | PXD000736 | Pride

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data