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10.1371/journal.ppat.1009753 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1009753 34260666!8312984!34260666     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2021 ; 17 (7): e1009753 Nephropedia Template TP {{tp|p=34260666|t=2021. COVID-19 virtual patient cohort suggests immune mechanisms driving disease outcomes |pdf=|usr=}}{{34260666}} gab.com Text COVID-19 virtual patient cohort suggests immune mechanisms driving disease outcomes JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34260666 #FOAvip To understand the diversity of immune responses to SARS-CoV-2 and distinguish features that predispose individuals to severe COVID-19, we developed a mechanistic, within-host mathematical model and virtual patient cohort. Our results suggest that virtual patients with low production rates of infected cell derived IFN subsequently experienced highly inflammatory disease phenotypes, compared to those with early and robust IFN responses. In these in silico patients, the maximum concentration of IL-6 was also a major predictor of CD8+ T cell depletion. Our analyses predicted that individuals with severe COVID-19 also have accelerated monocyte-to-macrophage differentiation mediated by increased IL-6 and reduced type I IFN signalling. Together, these findings suggest biomarkers driving the development of severe COVID-19 and support early interventions aimed at reducing inflammation. Twit Text FOAVip COVID-19 virtual patient cohort suggests immune mechanisms driving disease outcomes ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34260666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34260666 #FOAvip English Wikipedia <ref>{{Cite pmid|34260666}}</ref> COVID-19 virtual patient cohort suggests immune mechanisms driving disease outcomes #MMPMID34260666 Jenner AL; Aogo RA; Alfonso S; Crowe V; Deng X; Smith AP; Morel PA; Davis CL; Smith AM; Craig M PLoS Pathog 2021[Jul]; 17 (7): e1009753 PMID34260666show ga To understand the diversity of immune responses to SARS-CoV-2 and distinguish features that predispose individuals to severe COVID-19, we developed a mechanistic, within-host mathematical model and virtual patient cohort. Our results suggest that virtual patients with low production rates of infected cell derived IFN subsequently experienced highly inflammatory disease phenotypes, compared to those with early and robust IFN responses. In these in silico patients, the maximum concentration of IL-6 was also a major predictor of CD8+ T cell depletion. Our analyses predicted that individuals with severe COVID-19 also have accelerated monocyte-to-macrophage differentiation mediated by increased IL-6 and reduced type I IFN signalling. Together, these findings suggest biomarkers driving the development of severe COVID-19 and support early interventions aimed at reducing inflammation. |*Models, Immunological[MESH] |*SARS-CoV-2/immunology[MESH] |Biomarkers/metabolism[MESH] |CD8-Positive T-Lymphocytes/immunology[MESH] |COVID-19/*immunology/virology[MESH] |Cohort Studies[MESH] |Computational Biology[MESH] |Computer Simulation[MESH] |Disease Susceptibility/immunology[MESH] |Host Microbial Interactions/immunology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Immunosuppression Therapy[MESH] |Interferons/metabolism[MESH] |Interleukin-6/metabolism[MESH] |Macrophages/immunology[MESH] |Pandemics[MESH] |Severity of Illness Index[MESH]COVID-19 virtual patient cohort suggests immune mechanisms driving dis(epmc).pdf DeepDyve Pubget Overpricing