Pathogenesis of COVID-19-induced ARDS: implications for an ageing population
Open accessAbstract
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-γ 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.
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In severe COVID-19, ARDS usually begins around day 12 after symptom onset, when viral shedding is mostly resolved, and death or recovery follows about 7-12 days later.
“The onset of ARDS in severe cases typically occurs around day 12 post-symptom onset44,57, when viral shedding appears to be mostly resolved58, followed by death or recovery around 7-12 days later44,57.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [57]
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References 95 · Cited by 247
Research works printed but not linked: 1
- [72]Tang X, Du RH, Wang R, et al. Comparison of hospitalized patients with ARDS caused by COVID-19 and H1N1. Chest 2020; 158: 195– 205. doi: 10.1016/j.chest.2020.03.032 32224074 PMC7151343 · DOI
- Authors
- Torres Acosta, M. A., & Singer, B. D.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Singer, Benjamin D.
- Venue
- European Respiratory Journal
- Publisher
- European Respiratory Society (ERS)
- Published
- 2020-08-03
- Volume
- 56
- Issue
- 3
- Pages
- 2002049
- ISSN
- 0903-1936 (ISSN-L)
- 1399-3003
- PMC
- PMC7397945
- OpenAlex
- W3047405892
- Cited by
- 247
- References
- 95
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 24 · 2023: 42 · 2022: 70 · 2021: 77 · 2020: 9
- FWCI
- 6.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- European Respiratory Journal (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (P01AG049665)
- National Institute of General Medical Sciences (T32GM008152)
- National Heart, Lung, and Blood Institute (K08HL128867, R01HL149883)
- National Institute of Allergy and Infectious Diseases (U19AI135964)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- COVID-19 pandemic, SARS-CoV-2, acute respiratory distress syndrome, lung injury, viral pneumonia, influenza A virus, aging, host immune response, interferon-gamma, lymphopenia, host risk factors, age-related susceptibility
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Aging, Disease Susceptibility, Humans, Pneumonia, Viral, Respiratory Distress Syndrome, Virus Replication, Coronavirus Infections, Pandemics
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