A multiple-hit hypothesis involving reactive oxygen species and myeloperoxidase explains clinical deterioration and fatality in COVID-19
Open accessAbstract
Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality.The unique clinical phenomena in severe COVID-19 can be perplexing, and they include disproportionately severe hypoxemia relative to lung alveolar-parenchymal pathology and rapid clinical deterioration, with poor response to O2 supplementation, despite preserved lung mechanics.Factors such as microvascular injury, thromboembolism, pulmonary hypertension, and alteration in hemoglobin structure and function could play important roles.Overwhelming immune response associated with "cytokine storms" could activate reactive oxygen species (ROS), which may result in consumption of nitric oxide (NO), a critical vasodilation regulator.In other inflammatory infections, activated neutrophils are known to release myeloperoxidase (MPO) in a natural immune response, which contributes to production of hypochlorous acid (HOCl).However, during overwhelming inflammation, HOCl competes with O2 at heme binding sites, decreasing O2 saturation.Moreover, HOCl contributes to several oxidative reactions, including hemoglobin-heme iron oxidation, heme destruction, and subsequent release of free iron, which mediates toxic tissue injury through additional generation of ROS and NO consumption.Connecting these reactions in a multi-hit model can explain generalized tissue damage, vasoconstriction, severe hypoxia, and precipitous clinical deterioration in critically ill COVID-19 patients.Understanding these mechanisms is critical to develop therapeutic strategies to combat COVID-19.
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Reactive oxygen species and myeloperoxidase are implicated in clinical deterioration and mortality in COVID-19.
“A similar idea is maintained by Pravin T Goud et al., in developing an analysis implicating reactive oxygen species and myeloperoxidase in clinical deterioration and mortality in COVID-19 [164].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [164]
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- Authors
- Goud, P. T., Bai, D., & Abu-Soud, H. M.
- Affiliations
- California Northstate University (US)
- Wayne State University (US)
- Venue
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Published
- 2021
- Volume
- 17
- Issue
- 1
- Pages
- 62-72
- ISSN
- 1449-2288 (ISSN-L)
- PMC
- PMC7757048
- OpenAlex
- W3096758810
- Cited by
- 88
- References
- 131
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 13 · 2023: 16 · 2022: 25 · 2021: 18
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- International Journal of Biological Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- COVID-19 pandemic, reactive oxygen species, myeloperoxidase, hypochlorous acid, nitric oxide consumption, heme iron oxidation, free iron, neutrophils, cytokine storm, hypoxemia, clinical deterioration, multiple-hit model, oxidative stress, tissue damage, vasoconstriction
- MeSH terms
- Clinical Deterioration, COVID-19, SARS-CoV-2, Catalysis, Humans, Hypochlorous Acid, Peroxidase, Oxidation-Reduction, Reactive Oxygen Species
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