tetano
Editor, Senior Moderator
Indian J Pathol Microbiol
. 2023 Jan-Mar;66(1):19-23.
doi: 10.4103/ijpm.ijpm_734_21.
SARS-CoV-2 induced changes in the lungs based on autopsy cases
Mina Miroslavova Pencheva[SUP] 1 [/SUP], Sylvia Nikolaeva Genova[SUP] 2 [/SUP]
Affiliations
Abstract
Context: Researchers throughout the world devote enormous efforts to reveal the peculiarities of the pathogenesis of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, however, it continues to surprise and cause the death of millions of people.
Aims: This article aims to study the molecular mechanisms provoked by SARS-CoV-2, the virus-induced changes in Angiotensin-converting enzyme 2 (ACE2) functionality, in the vascular homeostasis through CD34 expression, B-cell immunity through the expression of CD20 and CD79α, and adhesion molecules through E-cadherin.
Settings and design: This was a prospective, descriptive, and observational study.
Methods and material: A total of 15 autopsies of patients deceased by COVID-19 infection, confirmed by PCR, were performed. The lungs of all patients were examined histologically and immunohistochemically for ACE2, E-cadherin, CD34, CD20, and CD79α.
Results: Immunohistological analysis showed increased ACE2 expression in all lung autopsy material affected by COVID-19 infection and we found a higher intensity of ACE2 expression than that of a healthy lung. CD20 examination reveals total deficiency of B-cells in the pulmonary parenchyma and CD79α is also absent. E-Cadherin is not expressed in the basal cellular sections where the contact elements are missing. CD34 demonstrates a desquamation of the endothelial cells, which indicates a direct damage of the vascular walls.
Conclusions: We found that patients who died after severe COVID-19 had high immune deficiency and impaired intercellular communication in the parenchyma and endothelium of lung tissue, leading to severe thromboembolic complications in patients with multiple diseases.
Keywords: Angiotensin-converting enzyme 2; COVID-19; SARS-CoV-2; respiratory diseases.
. 2023 Jan-Mar;66(1):19-23.
doi: 10.4103/ijpm.ijpm_734_21.
SARS-CoV-2 induced changes in the lungs based on autopsy cases
Mina Miroslavova Pencheva[SUP] 1 [/SUP], Sylvia Nikolaeva Genova[SUP] 2 [/SUP]
Affiliations
- PMID: 36656205
- DOI: 10.4103/ijpm.ijpm_734_21
Abstract
Context: Researchers throughout the world devote enormous efforts to reveal the peculiarities of the pathogenesis of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, however, it continues to surprise and cause the death of millions of people.
Aims: This article aims to study the molecular mechanisms provoked by SARS-CoV-2, the virus-induced changes in Angiotensin-converting enzyme 2 (ACE2) functionality, in the vascular homeostasis through CD34 expression, B-cell immunity through the expression of CD20 and CD79α, and adhesion molecules through E-cadherin.
Settings and design: This was a prospective, descriptive, and observational study.
Methods and material: A total of 15 autopsies of patients deceased by COVID-19 infection, confirmed by PCR, were performed. The lungs of all patients were examined histologically and immunohistochemically for ACE2, E-cadherin, CD34, CD20, and CD79α.
Results: Immunohistological analysis showed increased ACE2 expression in all lung autopsy material affected by COVID-19 infection and we found a higher intensity of ACE2 expression than that of a healthy lung. CD20 examination reveals total deficiency of B-cells in the pulmonary parenchyma and CD79α is also absent. E-Cadherin is not expressed in the basal cellular sections where the contact elements are missing. CD34 demonstrates a desquamation of the endothelial cells, which indicates a direct damage of the vascular walls.
Conclusions: We found that patients who died after severe COVID-19 had high immune deficiency and impaired intercellular communication in the parenchyma and endothelium of lung tissue, leading to severe thromboembolic complications in patients with multiple diseases.
Keywords: Angiotensin-converting enzyme 2; COVID-19; SARS-CoV-2; respiratory diseases.