The spike protein is the part of the virus structure that interfaces with the host cell. SARS 1 and SARS 2 (severe acute respiratory syndrome) viruses both have spike proteins that bind to a healthy human cell receptor called ACE-2 (angiotensin-converting enzyme), common in lung cells but also present in other parts of the body. Binding to the cell’s ACE-2 receptor is like the wolf knocking at the door of Little Red Riding Hood’s grandmother. “Hello, grandmama. I’m your granddaughter. Please let me in.” The virus is a wolf wearing a red cape and hood, pretends to be an ACE-2 enzyme molecule seeking entrance to the cell.
A paper published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level.
“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.” the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time.
In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in endothelial cells lining the pulmonary artery walls.
The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.
The research was supported by the National Institutes of Health, the National Natural Science Foundation of China, the Shaanxi Natural Science Fund, the National Key Research and Development Program, the First Affiliated Hospital of Xi’an Jiaotong University; and Xi’an Jiaotong University.
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