Pulmonary pathology of ARDS in COVID-19: A pathological review for clinicians
Open accessAbstract
COVID-19 has quickly reached pandemic levels since it was first reported in December 2019. The virus responsible for the disease, named SARS-CoV-2, is enveloped positive-stranded RNA viruses. During its replication in the cytoplasm of host cells, the viral genome is transcribed into proteins, such as the structural protein spike domain S1, which is responsible for binding to the cell receptor of the host cells. Infected patients have initially flu-like symptoms, rapidly evolving to severe acute lung injury, known as acute respiratory distress syndrome (ARDS). ARDS is characterized by an acute and diffuse inflammatory damage into the alveolar-capillary barrier associated with a vascular permeability increase and reduced compliance, compromising gas exchange and causing hypoxemia. Histopathologically, this condition is known as diffuse alveolar damage which consists of permanent damage to the alveoli epithelial cells and capillary endothelial cells, with consequent hyaline membrane formation and eventually intracapillary thrombosis. All of these mechanisms associated with COVID-19 involve the phenotypic expression from different proteins transcription modulated by viral infection in specific pulmonary microenvironments. Therefore, this knowledge is fundamentally important for a better pathophysiological understanding and identification of the main molecular pathways associated with the disease evolution. Evidently, clinical findings, signs and symptoms of a patient are the phenotypic expression of these pathophysiological and molecular mechanisms of SARS-CoV-2 infection. Therefore, no findings alone, whether molecular, clinical, radiological or pathological axis are sufficient for an accurate diagnosis. However, their intersection and/or correlation are extremely critical for clinicians establish the diagnosis and new treatment perspectives.
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Viral infection is mediated mainly by the binding of SARS-CoV-2 to the ACE2 receptor expressed on the surface of lung epithelial cells, endothelium, pericytes, and other cell types.
“Viral infection is mediated mainly by the binding of SARS-CoV-2 to the angiotensin–converting enzyme 2 (ACE2) receptor expressed on the surface of lung epithelial cells, endothelium, pericytes, and other cell types (1–4).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [1]
The major reported lung pathologies of severe COVID-19 include diffuse alveolar damage, organizing pneumonia, and chronic interstitial pneumonia.
“The major reported lung pathologies of severe COVID-19 include diffuse alveolar damage (DAD), organizing pneumonia, and chronic interstitial pneumonia (1–3, 5).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [1]
DAD and alveolar-capillary barrier breakdown are prominent pathological features of severe COVID-19.
“DAD and alveolar-capillary barrier breakdown are prominent pathological features of severe COVID-19 (1–4).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [1]
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- Authors
- Batah, S. S., & Fabro, A. T.
- Affiliations
- Universidade de São Paulo (BR)
- Corresponding author
- Fabro, Alexandre Todorovic
- Venue
- Respiratory Medicine
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 176
- Pages
- 106239
- ISSN
- 0954-6111 (ISSN-L)
- PMC
- PMC7674971
- OpenAlex
- W3104639833
- Cited by
- 319
- References
- 58
- Citations by year
- 2026: 8 · 2025: 31 · 2024: 52 · 2023: 81 · 2022: 88 · 2021: 57 · 2020: 1
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 730 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Respiratory Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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 pathology, diffuse alveolar damage, hyaline membrane formation, vascular permeability, hypoxemia, lung histopathology, pathophysiology
- MeSH terms
- COVID-19, SARS-CoV-2, Humans, Respiratory Distress Syndrome
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