About: 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.   Goto Sponge  NotDistinct  Permalink

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  • 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.
subject
  • Animal physiology
  • Patent law
  • 19th century in San Jose, California
  • Defunct California railroads
  • History of San Francisco
  • Mission District, San Francisco
  • Railway companies disestablished in 1870
  • Railway companies established in 1860
  • Transportation in the San Francisco Bay Area
  • Predecessors of the Southern Pacific Transportation Company
  • 1863 establishments in California
  • 1870 disestablishments in California
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