The SARS-CoV-2 S protein alters cardiac PC function (Technical)

 This is a technical but important article which confirms why inflammatory cytokines are produced and why the vaccine may consequently induce heart and micro-vascular diseases. (You will find the full article in the link below.)

 A research team led by Bristol's Professor Paolo Madeddu exposed human heart pericytes, which are cells that wrap small blood vessels in the heart, to SARS-CoV-2 Alpha and Delta variants, along with the original Wuhan virus. Surprisingly, they found the heart pericytes were not infected.

Intrigued by this finding, in a second test-tube experiment, the researchers challenged the cardiac pericytes with the spike protein alone, without the virus. The spike protein made pericytes unable to interact with their companion endothelial cells and induced them to secrete inflammatory cytokines, suggesting the spike protein is harmful to human cardiac cells. Interestingly, the team found that antibodies blocking CD147 — a receptor for the spike protein — protected heart pericytes from damage.

Schematic summary of the research. We hypothesise that in patients with acute COVID-19, S protein molecules are cleaved from the virus particle and released from the respiratory system into the bloodstream. Through the circulation, isolated S protein reaches all organs of the body, including the heart. Here, the interaction of the S protein with the CD147 receptor on cardiac PCs triggers the ERK1/2 signalling (A) and provokes PC dysfunction, including increased cell motility (B) and decreased cooperation with coronary ECs during angiogenesis. (C). In addition, the S protein–CD147 interaction prompts cardiac PCs to release pro-apoptotic factors, which cause EC death (D). Finally, through a mechanism CD147-independent, the S protein induces PCs to release pro-inflammatory cytokines, which include MCP1, IL-6, IL-1β, and TNFα (E). These cytokines can damage neighbouring cardiomyocytes and activate ECs, potentially triggering blood clotting and increasing vascular permeability.