SARS-CoV-2 induced changes in the lungs based on autopsy cases.

Area of Science:

• Pathology
• Immunology
• Molecular Biology

Background:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pathogenesis remains incompletely understood despite significant global research efforts.
• The virus continues to cause widespread mortality and presents ongoing challenges in understanding its complex mechanisms.

Purpose of the Study:

• To investigate the molecular mechanisms underlying SARS-CoV-2 infection.
• To examine virus-induced alterations in Angiotensin-converting enzyme 2 (ACE2) functionality.
• To assess impacts on vascular homeostasis (CD34), B-cell immunity (CD20, CD79α), and cell adhesion (E-cadherin).

Main Methods:

• Prospective, descriptive, observational study design.
• Histological and immunohistochemical analysis of lung autopsy material from 15 patients deceased from COVID-19.
• Evaluation of ACE2, E-cadherin, CD34, CD20, and CD79α expression.

Main Results:

• Increased ACE2 expression observed in COVID-19 lung tissue compared to healthy lungs.
• Complete deficiency of B-cells (CD20, CD79α) in pulmonary parenchyma.
• Absence of E-cadherin in basal cellular sections, indicating loss of cell-cell contact.
• CD34 expression indicated endothelial cell desquamation and direct vascular wall damage.

Conclusions:

• Patients deceased from severe COVID-19 exhibited significant immune deficiency.
• Impaired intercellular communication in lung parenchyma and endothelium was noted.
• These molecular and cellular changes contribute to severe thromboembolic complications in patients with comorbidities.