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Updated: Dec 21, 2025
Lung CT Segmentation to Identify Consolidations and Ground Glass Areas for Quantitative Assesment of SARS-CoV Pneumonia
Published on: December 19, 2020
Clinical and pathological investigation of patients with severe COVID-19
Shaohua Li1, Lina Jiang1, Xi Li1
1Department of Pathology and Hepatology.
Insights
Elevated cytokines like IL-6 and IL-8 indicate severe COVID-19 progression. Understanding SARS-CoV-2 infection and immune responses is key to improving patient outcomes.
Area of Science:
- Immunology
- Virology
- Pathology
Background:
- COVID-19 pandemic caused by SARS-CoV-2.
- Study focuses on clinical and immunopathological features of severe COVID-19.
Purpose of the Study:
- Analyze clinical and laboratory characteristics of severe COVID-19 patients.
- Investigate cytokine profiles and immunopathology in severe cases.
Main Methods:
- Classified 69 COVID-19 patients into severe and non-severe groups.
- Quantified blood cytokines over time.
- Examined biopsy specimens from deceased patients.
Main Results:
- Severe COVID-19 showed elevated IL-8, IL-6, TNF-α, IP10, MCP1, and RANTES.
- SARS-CoV-2 infected pneumocytes and endothelial cells, causing lung damage via pyroptosis and apoptosis.
- Observed lymphopenia, neutrophilia, T-cell depletion, and inflammatory cell infiltrates in severe cases.
Conclusions:
- Circulating cytokines can predict disease progression and guide interventions.
- Severe lung damage results from viral cytopathy and immunopathology.
- Targeting cytokine storm may improve outcomes in severe COVID-19.
Background:
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), has become a pandemic. This study addresses the clinical and immunopathological characteristics of severe COVID-19.
Methods:
Sixty-nine patients with COVID-19 were classified into severe and nonsevere groups to analyze their clinical and laboratory characteristics. A panel of blood cytokines was quantified over time. Biopsy specimens from 2 deceased cases were obtained for immunopathological, ultrastructural, and in situ hybridization examinations.
Results:
Circulating cytokines, including IL-8, IL-6, TNF-α, IP10, MCP1, and RANTES, were significantly elevated in patients with severe COVID-19. Dynamic IL-6 and IL-8 were associated with disease progression. SARS-CoV-2 was demonstrated to infect type II and type I pneumocytes and endothelial cells, leading to severe lung damage through cell pyroptosis and apoptosis. In severe cases, lymphopenia, neutrophilia, depletion of CD4+ and CD8+ T lymphocytes, and massive macrophage and neutrophil infiltrates were observed in both blood and lung tissues.
Conclusions:
A panel of circulating cytokines could be used to predict disease deterioration and inform clinical interventions. Severe pulmonary damage was predominantly attributed to both cytopathy caused by SARS-CoV-2 and immunopathologic damage. Strategies that prohibit pulmonary recruitment and overactivation of inflammatory cells by suppressing cytokine storm might improve the outcomes of patients with severe COVID-19.
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