Author: Yafei Wang; Randy Heiland; Morgan Craig; Courtney L. Davis; Ashlee N Ford Versypt; Adrianne Jenner; Jonathan Ozik; Nicholson Collier; Chase Cockrell; Andrew Becker; Gary An; James A. Glazier; Aarthi Narayanan; Amber M Smith; Paul Macklin
Title: Rapid community-driven development of a SARS-CoV-2 tissue simulator Document date: 2020_4_5
ID: lq4tcyh4_71
Snippet: While the underlying risk-factors for an individual developing acute respiratory distress syndrome (ARDS) in response to SARS-CoV-2 infection have not yet been elucidated, it appears clear that a dysregulated immune response is central to this aspect of the disease 2,3,25,40 . In particular, chemokines are released following viral infection, which leads to the invasion of neutrophils and macrophages and release of reactive oxygen species (ROS). I.....
Document: While the underlying risk-factors for an individual developing acute respiratory distress syndrome (ARDS) in response to SARS-CoV-2 infection have not yet been elucidated, it appears clear that a dysregulated immune response is central to this aspect of the disease 2,3,25,40 . In particular, chemokines are released following viral infection, which leads to the invasion of neutrophils and macrophages and release of reactive oxygen species (ROS). In addition, replication in the lower airways and exposure of endothelial cells may further amplify the inflammatory response 32 . Collectively, this leads to extensive tissue damage and depletion of epithelial cells, which may be connected to lethality 41 . Within the alveolar tissue, and systemically, the feedback between viral load, adaptive and innate immune response and tissue damage is clearly a complex system. By utilizing a multi-scale framework to implement these interactions, we aim to connect circulating biomarkers, putative treatments, and clinically observed disease progression to pathophysiological changes at the cell and tissue level.
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