Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glycerophospholipid remodeling is critical for orthoflavivirus infection

ABSTRACT: Glycerophospholipid remodeling is critical for orthoflavivirus infection

PROVIDER: PRJNA1101937 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Glycerophospholipid remodeling is critical for orthoflavivirus infection

Project description:Flavivirus infection is tightly connected to host lipid metabolism. Here, we performed shotgun lipidomics of cells infected with neurotropic Zika, West Nile, and tick-borne encephalitis viruses, as well as dengue and yellow fever virus. Early in infection specific lipids accumulated, e.g., neutral lipids in Zika and some lyso-phospholipids in all infections. Ceramide levels increased following infection with viruses that cause a cytopathic effect. In addition, fatty acid desaturation as well as glycerophospholipid metabolism were significantly altered. Importantly, depletion of enzymes involved in phosphatidylserine metabolism as well as phosphatidylinositol biosynthesis reduced orthoflavivirus titers and cytopathic effects while inhibition of fatty acid monounsaturation only rescued from virus-induced cell death. Interestingly, interfering with ceramide synthesis had opposing effects on virus replication and cytotoxicity depending on the targeted enzyme. Thus, lipid remodeling by orthoflaviviruses includes distinct changes but also common patterns shared by several viruses that are needed for efficient infection and replication.

2024-09-03 | GSE264306 | GEO

Chromatin remodeling protein HELLS is critical for retinoblastoma tumor initiation and progression

Project description:Chromatin remodeling protein HELLS is critical for retinoblastoma tumor initiation and progression

| PRJNA603598 | ENA

Mitochondrial-derived glutamate dictates resistance to pathogen infection through vitamin-dependent metabolic remodeling

Project description:The functional integration of innate immune and metabolic signaling responses represents an ancient strategy to manage infections in metazoans. Using Drosophila, we uncovered that immune-metabolic sensing in muscle dictates resistance to enteric bacterial infection through vitamins dependent metabolic remodeling. Within muscle, the activation strength of systemic innate immune signaling, integrated with mitochondrial-dependent glutamate dehydrogenase (Gdh) function, conditions lipid mobilization from adipose. Mild intramuscular IMD/innate immune signaling activity allows for infection-mediated increases in mitochondrial biogenesis/function, which further stimulates mitochondria/Gdh-dependent synthesis of glutamate. Intramuscular derived glutamate acts as a systemic metabolite to influence lipid mobilization through altering vitamin metabolism. This lipid mobilization improves bacterial clearance and boost infection resistance. Conversely, elevated activation of IMD/innate immune signaling in muscle impedes infection-mediated increases in mitochondrial biogenesis/function and subsequent metabolic remodeling. Finally, life history traits that fine-tune intramuscular mitochondrial dynamics consequently influence infection resistance and shape phenotypic diversity of infection responses within populations.

2021-11-19 | GSE160652 | GEO

Influenza virus infection leads to global cardiac proteome remodeling during convalescence

Project description:Influenza virus infection leads to global cardiac proteome remodeling during convalescence MTD project_description "Influenza virus infections lead to more than 500,000 hospitalizations in the U.S. every year. Patients with cardiovascular diseases have been shown to be at high risk of influenza mediated cardiac complications. Importantly, recent reports have provided clinical data supporting a direct link between laboratory-confirmed influenza virus infection and adverse cardiac events. However, the molecular mechanisms of how influenza virus infection induces detrimental cardiac changes, even after resolution of the pulmonary infection, is completely unknown.

2022-04-01 | PXD015992 | Pride

Epithelial Plasticity and Innate Immune Activation Promote Lung Tissue Remodeling following Respiratory Viral Infection.

Project description:As observed in mice with genetic depletion of stem cells, epithelial plasticity is a critical component of tissue repair in response to injury; however, the physiological relevance of this process and the involved progenitor populations are not well understood. Severe respiratory viral infection and chronic lung disease share pathological features including stem cell loss in the gas-exchange regions, basal cell (BC) hyperplasia in small airways, and innate immune activation. Collectively, these processes contribute to epithelial remodeling and loss of diffusion capacity. Here, we show that small airways harbor a previously undescribed lineage of secretory cells, intralobar serous (IS) cells, that are activated to assume BC fates following influenza virus infection. Nascent BC were distinguished from pre-existing BC by high expression of IL-22Ra1 and a dependency on innate immune activation and local IL-22 production for self-renewal and colonization of injured alveoli. Resolution of virus-elicited inflammation and the associated decline in IL-22 signaling resulted in basal to serous re-differentiation in repopulated alveoli, and increased local expression of antimicrobial factors, but failed to replace normal alveolar epithelium. We define a mechanism whereby epithelial plasticity confers protection against mortality from acute respiratory viral infection but has potential to contribute to progressive lung remodeling and life-threatening declines in lung function among patients with chronic lung disease.

2023-08-08 | GSE184384 | GEO

Influenza virus infection leads to global cardiac proteome remodeling during convalescence

2022-04-04 | PXD016412 | Pride

Motor neurons use push-pull signals to direct vascular remodeling critical for their connectivity

Project description:Motor neurons use push-pull signals to direct vascular remodeling critical for their connectivity

| PRJNA857720 | ENA

The dynamics of Cryptococcus neoformans cell and transcriptional remodeling during infection

Project description:The dynamics of Cryptococcus neoformans cell and transcriptional remodeling during infection

| PRJNA851987 | ENA

Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection

Project description:Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection

| PRJNA980098 | ENA

Spatiotemporal transcriptome analysis reveals critical roles for mechano-sensing genes at the border zone in remodeling after myocardial infarction

Project description:The underlying mechanisms of ventricular remodeling after myocardial infarction (MI) remain largely unknown. Here, we performed an integrative analysis of spatial transcriptomics and single-nucleus RNA-seq in a murine MI model and found that mechanical stress-response genes are expressed at the border zone and play a critical role in left ventricular remodeling following MI. An integrative analysis of single-nucleus RNA-seq and spatial transcriptome of the heart tissue after MI identified the unique cluster that appeared at the border zone in an early stage, highly expressing mechano-sensing genes such as Csrp3. AAV9-mediated gene silencing and overexpression of Csrp3 demonstrated that upregulation of Csrp3 plays critical roles in preventing cardiac remodeling after MI via regulation of genes associated with mechano-sensing. Overall, our study not only provides an insight into spatiotemporal molecular changes following MI but also highlights that the mechano-sensing genes at the border zone act as adaptive regulators of left ventricular remodeling.

2022-07-25 | GSE176092 | GEO

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