Department of Medical Physics and Biophysics, Faculty of Pharmacy, Medical University of Plovdiv, Plovdiv, Bulgaria.
Department of General and Clinical Pathology, Faculty of Medicine, Medical University of Plovdiv; University Multiprofile Hospital for Active Medical Treatment "Sveti Georgi"EAD, Plovdiv, Bulgaria.
Indian J Pathol Microbiol. 2023 Jan-Mar;66(1):19-23. doi: 10.4103/ijpm.ijpm_734_21.
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.
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.
This was a prospective, descriptive, and observational study.
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.
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.
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.
世界各地的研究人员都在努力揭示严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）病毒发病机制的特殊性，但它仍在不断出现并导致数百万人死亡。
本文旨在研究 SARS-CoV-2 引发的分子机制，病毒诱导的血管内环境平衡中血管紧张素转换酶 2（ACE2）功能的改变，通过 CD34 表达引起的血管内皮细胞功能改变，B 细胞免疫通过 CD20 和 CD79α 的表达，以及通过 E-钙黏蛋白引起的黏附分子改变。
这是一项前瞻性、描述性和观察性研究。
对 15 例经 PCR 证实死于 COVID-19 感染的患者进行了尸检。所有患者的肺均进行了组织学和免疫组织化学检查，以检查 ACE2、E-钙黏蛋白、CD34、CD20 和 CD79α。
免疫组织化学分析显示，所有受 COVID-19 感染影响的肺尸检材料中 ACE2 表达增加，我们发现 ACE2 表达的强度高于健康肺。CD20 检查显示肺实质中的 B 细胞完全缺乏，CD79α 也不存在。E-钙黏蛋白在接触元件缺失的基底细胞节段不表达。CD34 显示内皮细胞的剥落，这表明血管壁直接受损。
我们发现，死于严重 COVID-19 的患者存在高免疫缺陷，肺组织实质和内皮细胞的细胞间通讯受损，导致患有多种疾病的患者发生严重的血栓栓塞并发症。
