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10.1016/j.ebiom.2020.102887

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suck abstract from ncbi


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pmid32736307      EBioMedicine 2020 ; 58 (ä): 102887
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  • The four horsemen of a viral Apocalypse: The pathogenesis of SARS-CoV-2 infection (COVID-19) #MMPMID32736307
  • Domingo P; Mur I; Pomar V; Corominas H; Casademont J; de Benito N
  • EBioMedicine 2020[Aug]; 58 (ä): 102887 PMID32736307show ga
  • The pathogenesis of coronavirus disease 2019 (COVID-19) may be envisaged as the dynamic interaction between four vicious feedback loops chained or happening at once. These are the viral loop, the hyperinflammatory loop, the non-canonical renin-angiotensin system (RAS) axis loop, and the hypercoagulation loop. Severe acute respiratory syndrome (SARS)-coronavirus (CoV)-2 lights the wick by infecting alveolar epithelial cells (AECs) and downregulating the angiotensin converting enzyme-2 (ACE2)/angiotensin (Ang-1-7)/Mas1R axis. The viral feedback loop includes evading the host's innate response, uncontrolled viral replication, and turning on a hyperactive adaptative immune response. The inflammatory loop is composed of the exuberant inflammatory response feeding back until exploding in an actual cytokine storm. Downregulation of the ACE2/Ang-(1-7)/Mas1R axis leaves the lung without a critical defense mechanism and turns the scale to the inflammatory side of the RAS. The coagulation loop is a hypercoagulable state caused by the interplay between inflammation and coagulation in an endless feedback loop. The result is a hyperinflammatory and hypercoagulable state producing acute immune-mediated lung injury and eventually, adult respiratory distress syndrome.
  • |*Blood Coagulation[MESH]
  • |*Renin-Angiotensin System[MESH]
  • |Animals[MESH]
  • |Betacoronavirus/*pathogenicity[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*etiology/metabolism/pathology/virology[MESH]
  • |Cytokines/*metabolism[MESH]
  • |Feedback, Physiological[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*etiology/metabolism/pathology/virology[MESH]


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