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10.1016/j.mcpro.2021.100159 http://scihub22266oqcxt.onion/10.1016/j.mcpro.2021.100159 34619366!8490130!34619366     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34619366&cmd=llinks): Failed to open stream: HTTP request failed! 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Metabolic Perturbation Associated With COVID-19 Disease Severity and SARS-CoV-2 Replication |pdf=|usr=}}{{34619366}} gab.com Text Metabolic Perturbation Associated With COVID-19 Disease Severity and SARS-CoV-2 Replication JO: Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=34619366 #FOAvip Viruses hijack host metabolic pathways for their replicative advantage. In this study, using patient-derived multiomics data and in vitro infection assays, we aimed to understand the role of key metabolic pathways that can regulate severe acute respiratory syndrome coronavirus-2 reproduction and their association with disease severity. We used multiomics platforms (targeted and untargeted proteomics and untargeted metabolomics) on patient samples and cell-line models along with immune phenotyping of metabolite transporters in patient blood cells to understand viral-induced metabolic modulations. We also modulated key metabolic pathways that were identified using multiomics data to regulate the viral reproduction in vitro. Coronavirus disease 2019 disease severity was characterized by increased plasma glucose and mannose levels. Immune phenotyping identified altered expression patterns of carbohydrate transporter, glucose transporter 1, in CD8(+) T cells, intermediate and nonclassical monocytes, and amino acid transporter, xCT, in classical, intermediate, and nonclassical monocytes. In in vitro lung epithelial cell (Calu-3) infection model, we found that glycolysis and glutaminolysis are essential for virus replication, and blocking these metabolic pathways caused significant reduction in virus production. Taken together, we therefore hypothesized that severe acute respiratory syndrome coronavirus-2 utilizes and rewires pathways governing central carbon metabolism leading to the efflux of toxic metabolites and associated with disease severity. Thus, the host metabolic perturbation could be an attractive strategy to limit the viral replication and disease severity. Twit Text FOAVip Metabolic Perturbation Associated With COVID-19 Disease Severity and SARS-CoV-2 Replication ????Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=34619366 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34619366 #FOAvip English Wikipedia <ref>{{Cite pmid|34619366}}</ref> Metabolic Perturbation Associated With COVID-19 Disease Severity and SARS-CoV-2 Replication #MMPMID34619366 Krishnan S; Nordqvist H; Ambikan AT; Gupta S; Sperk M; Svensson-Akusjarvi S; Mikaeloff F; Benfeitas R; Saccon E; Ponnan SM; Rodriguez JE; Nikouyan N; Odeh A; Ahlen G; Asghar M; Sallberg M; Vesterbacka J; Nowak P; Vegvari A; Sonnerborg A; Treutiger CJ; Neogi U Mol Cell Proteomics 2021[]; 20 (ä): 100159 PMID34619366show ga Viruses hijack host metabolic pathways for their replicative advantage. In this study, using patient-derived multiomics data and in vitro infection assays, we aimed to understand the role of key metabolic pathways that can regulate severe acute respiratory syndrome coronavirus-2 reproduction and their association with disease severity. We used multiomics platforms (targeted and untargeted proteomics and untargeted metabolomics) on patient samples and cell-line models along with immune phenotyping of metabolite transporters in patient blood cells to understand viral-induced metabolic modulations. We also modulated key metabolic pathways that were identified using multiomics data to regulate the viral reproduction in vitro. Coronavirus disease 2019 disease severity was characterized by increased plasma glucose and mannose levels. Immune phenotyping identified altered expression patterns of carbohydrate transporter, glucose transporter 1, in CD8(+) T cells, intermediate and nonclassical monocytes, and amino acid transporter, xCT, in classical, intermediate, and nonclassical monocytes. In in vitro lung epithelial cell (Calu-3) infection model, we found that glycolysis and glutaminolysis are essential for virus replication, and blocking these metabolic pathways caused significant reduction in virus production. Taken together, we therefore hypothesized that severe acute respiratory syndrome coronavirus-2 utilizes and rewires pathways governing central carbon metabolism leading to the efflux of toxic metabolites and associated with disease severity. Thus, the host metabolic perturbation could be an attractive strategy to limit the viral replication and disease severity. |Adult[MESH] |Aged[MESH] |Amino Acid Transport System y+/blood[MESH] |Amino Acids/blood[MESH] |Biomarkers/blood[MESH] |Blood Proteins/analysis/*metabolism[MESH] |COVID-19/*etiology/metabolism/virology[MESH] |Carbohydrates/blood[MESH] |Case-Control Studies[MESH] |Glucose Transporter Type 1/blood[MESH] |Hospitalization[MESH] |Humans[MESH] |Immunophenotyping[MESH] |Mannose-Binding Lectin/blood[MESH] |Mannose/blood[MESH] |Middle Aged[MESH] |SARS-CoV-2/*physiology[MESH] |Severity of Illness Index[MESH]Metabolic Perturbation Associated With COVID-19 Disease Severity and S(epmc).pdf DeepDyve Pubget Overpricing