The trinity of COVID-19: immunity, inflammation and intervention
Open accessAbstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic. Alongside investigations into the virology of SARS-CoV-2, understanding the fundamental physiological and immunological processes underlying the clinical manifestations of COVID-19 is vital for the identification and rational design of effective therapies. Here, we provide an overview of the pathophysiology of SARS-CoV-2 infection. We describe the interaction of SARS-CoV-2 with the immune system and the subsequent contribution of dysfunctional immune responses to disease progression. From nascent reports describing SARS-CoV-2, we make inferences on the basis of the parallel pathophysiological and immunological features of the other human coronaviruses targeting the lower respiratory tract - severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). Finally, we highlight the implications of these approaches for potential therapeutic interventions that target viral infection and/or immunoregulation.
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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 [58]
ROS increase with age because of mitochondrial dysfunction and inflammation, can drive NLRP3 inflammasome activation, and likely contribute further to COVID-19 pathophysiology in the elderly.
“ROS increase with age due to mitochondrial dysfunction and inflammation, and can also drive NLRP3 inflammasome activation, likely further contributing to COVID-19 pathophysiology in the elderly58,76,77.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [58]
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- Authors
- Tay, M. Z., Poh, C. M., Rénia, L., MacAry, P. A., & Ng, L. F. P.
- Affiliations
- Agency for Science, Technology and Research (SG)
- National University of Singapore (SG)
- Corresponding author
- Rénia, Laurent
- MacAry, Paul A.
- Ng, Lisa F. P.
- Venue
- Nature Reviews Immunology
- Published
- 2020-04-28
- Volume
- 20
- Issue
- 6
- Pages
- 363-374
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC7187672
- OpenAlex
- W3018517500
- Cited by
- 4,360
- References
- 136
- Citations by year
- 2026: 82 · 2025: 169 · 2024: 320 · 2023: 552 · 2022: 899 · 2021: 1369 · 2020: 961 · 2015: 1 · 2013: 1 · 2012: 1
- FWCI
- 44.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion)
- Funders
- Medical Research Council
- Biomedical Research Council
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- SARS-CoV-2, COVID-19 pandemic, immune response, inflammation, pathophysiology, immune dysregulation, SARS-CoV, MERS-CoV, lower respiratory tract infection, immune regulation, antiviral therapy, therapeutic interventions
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Animals, Humans, Inflammation, Pneumonia, Viral, Coronavirus Infections, Disease Progression, Pandemics
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