ArticleJournal of the Royal Society, Interface2021
Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19.
Article in Journal of the Royal Society, Interface, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Stability of a delayed SARS-CoV-2 reactivation model with logistic growth and adaptive immune response.Physica A · 2023Article
- The race to understand immunopathology in COVID-19: Perspectives on the impact of quantitative approaches to understand within-host interactions.Immunoinformatics (Amsterdam, Netherlands) · 2023Review
- Drug Cocktail Formulation via Circuit Design.IEEE transactions on molecular, biological, and multi-scale communications · 2023Article
- Development of a novel mathematical model that explains SARS-CoV-2 infection dynamics in Caco-2 cells.PeerJ · 2023Article
- Inhaled corticosteroids for the treatment of COVID-19.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Article
- Stem cell therapy for COVID-19 pneumonia.Molecular biomedicine · 2022Review
- Global analysis of within-host SARS-CoV-2/HIV coinfection model with latency.European physical journal plus · 2022Article
- Virgin coconut oil is effective in lowering C-reactive protein levels among suspect and probable cases of COVID-19.Journal of functional foods · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While the pathological mechanisms in COVID-19 illness are still poorly understood, it is increasingly clear that high levels of pro-inflammatory mediators play a major role in clinical deterioration in patients with severe disease. Current evidence points to a hyperinflammatory state as the driver of respiratory compromise in severe COVID-19 disease, with a clinical trajectory resembling acute respiratory distress syndrome, but how this 'runaway train' inflammatory response emerges and is maintained is not known. Here, we present the first mathematical model of lung hyperinflammation due to SARS-CoV-2 infection. This model is based on a network of purported mechanistic and physiological pathways linking together five distinct biochemical species involved in the inflammatory response. Simulations of our model give rise to distinct qualitative classes of COVID-19 patients: (i) individuals who naturally clear the virus, (ii) asymptomatic carriers and (iii-v) individuals who develop a case of mild, moderate, or severe illness. These findings, supported by a comprehensive sensitivity analysis, point to potential therapeutic interventions to prevent the emergence of hyperinflammation. Specifically, we suggest that early intervention with a locally acting anti-inflammatory agent (such as inhaled corticosteroids) may effectively blockade the pathological hyperinflammatory reaction as it emerges.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.