tetano
Editor, Senior Moderator
Eur Respir J
. 2020 Aug 3;2002049.
doi: 10.1183/13993003.02049-2020. Online ahead of print.
Pathogenesis of COVID-19-induced ARDS: implications for an aging population
Manuel A Torres Acosta[SUP] 1 [/SUP], Benjamin D Singer[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
The coronavirus disease (COVID)-19 pandemic has elicited a swift response by the scientific community to elucidate the pathogenesis of severe acute respiratory syndrome coronavirus (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 COVID-19's protean clinical presentation and associated lymphopenia, the contrasting role of interferon-γ in mediating the host immune response to these viruses, and SARS-CoV-2's tropism for vascular endothelial cells, commenting on the potential limitations of influenza as a model for COVID-19. Finally, we explore hallmarks of aging that could explain the association between advanced age and susceptibility to severe COVID-19.
. 2020 Aug 3;2002049.
doi: 10.1183/13993003.02049-2020. Online ahead of print.
Pathogenesis of COVID-19-induced ARDS: implications for an aging population
Manuel A Torres Acosta[SUP] 1 [/SUP], Benjamin D Singer[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 32747391
- DOI: 10.1183/13993003.02049-2020
Abstract
The coronavirus disease (COVID)-19 pandemic has elicited a swift response by the scientific community to elucidate the pathogenesis of severe acute respiratory syndrome coronavirus (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 COVID-19's protean clinical presentation and associated lymphopenia, the contrasting role of interferon-γ in mediating the host immune response to these viruses, and SARS-CoV-2's tropism for vascular endothelial cells, commenting on the potential limitations of influenza as a model for COVID-19. Finally, we explore hallmarks of aging that could explain the association between advanced age and susceptibility to severe COVID-19.