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10.1183/13993003.02049-2020 http://scihub22266oqcxt.onion/10.1183/13993003.02049-2020 32747391!7397945!32747391     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+Respir+J 2020 ; 56 (3): ä Nephropedia Template TP {{tp|p=32747391|t=2020. Pathogenesis of COVID-19-induced ARDS: implications for an ageing population |pdf=|usr=}}{{32747391}} gab.com Text Pathogenesis of COVID-19-induced ARDS: implications for an ageing population JO: Eur Respir J http://www.kidney.de/pget.php?&tw=1&pmid=32747391 #FOAvip The coronavirus disease 2019 (COVID-19) pandemic has elicited a swift response by the scientific community to elucidate the pathogenesis of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)-induced lung injury and develop effective therapeutics. Clinical data indicate that severe COVID-19 most commonly manifests as viral pneumonia-induced acute respiratory distress syndrome (ARDS), a clinical entity mechanistically understood best in the context of influenza A virus-induced pneumonia. Similar to influenza, advanced age has emerged as the leading host risk factor for developing severe COVID-19. In this review we connect the current understanding of the SARS-CoV-2 replication cycle and host response to the clinical presentation of COVID-19, borrowing concepts from influenza A virus-induced ARDS pathogenesis and discussing how these ideas inform our evolving understanding of COVID-19-induced ARDS. We also consider important differences between COVID-19 and influenza, mainly the protean clinical presentation and associated lymphopenia of COVID-19, the contrasting role of interferon-gamma in mediating the host immune response to these viruses, and the tropism for vascular endothelial cells of SARS-CoV-2, commenting on the potential limitations of influenza as a model for COVID-19. Finally, we explore hallmarks of ageing that could explain the association between advanced age and susceptibility to severe COVID-19. Twit Text FOAVip Pathogenesis of COVID-19-induced ARDS: implications for an ageing population ????Eur Respir J http://www.kidney.de/pget.php?&tw=1&pmid=32747391 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32747391 #FOAvip English Wikipedia <ref>{{Cite pmid|32747391}}</ref> Pathogenesis of COVID-19-induced ARDS: implications for an ageing population #MMPMID32747391 Torres Acosta MA; Singer BD Eur Respir J 2020[Sep]; 56 (3): ä PMID32747391show ga The coronavirus disease 2019 (COVID-19) pandemic has elicited a swift response by the scientific community to elucidate the pathogenesis of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)-induced lung injury and develop effective therapeutics. Clinical data indicate that severe COVID-19 most commonly manifests as viral pneumonia-induced acute respiratory distress syndrome (ARDS), a clinical entity mechanistically understood best in the context of influenza A virus-induced pneumonia. Similar to influenza, advanced age has emerged as the leading host risk factor for developing severe COVID-19. In this review we connect the current understanding of the SARS-CoV-2 replication cycle and host response to the clinical presentation of COVID-19, borrowing concepts from influenza A virus-induced ARDS pathogenesis and discussing how these ideas inform our evolving understanding of COVID-19-induced ARDS. We also consider important differences between COVID-19 and influenza, mainly the protean clinical presentation and associated lymphopenia of COVID-19, the contrasting role of interferon-gamma in mediating the host immune response to these viruses, and the tropism for vascular endothelial cells of SARS-CoV-2, commenting on the potential limitations of influenza as a model for COVID-19. Finally, we explore hallmarks of ageing that could explain the association between advanced age and susceptibility to severe COVID-19. |Aging/*physiology[MESH] |Betacoronavirus/*physiology[MESH] |COVID-19[MESH] |Coronavirus Infections/*complications[MESH] |Disease Susceptibility[MESH] |Humans[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications[MESH] |Respiratory Distress Syndrome/*virology[MESH] |SARS-CoV-2[MESH]Pathogenesis of COVID-19-induced ARDS: implications for an ageing popu(epmc).pdf DeepDyve Pubget Overpricing