Rochelle Walensky, former director of the U.S. Centers for Disease Control and Prevention (CDC), stated on “Good Morning America” in June 2021 that myocarditis cases are “really quite rare … minor, self-limited, they generally resolve with rest and standard medications.” However, this assertion was made based on a preliminary review of 300 cases and before conducting long-term follow-up.
A study published on Aug. 1 followed 40 adolescents in Hong Kong for up to a year. Follow-up testing performed in 26 patients with initial abnormal findings revealed that 58 percent of those with vaccine-associated myocarditis had persistent heart muscle scarring. The authors concluded: “There exists a potential long-term effect on exercise capacity and cardiac functional reserve during stress.”
This series demonstrates how exposure to the spike protein results in downstream cardiovascular issues. Given that vaccination causes the body to produce more spike protein, it is clear that additional research was needed to understand the health impacts of vaccination prior to licensure.
Summary of Key Facts
- The SARS-CoV-2 spike protein and its S1 subunit have known impacts on the cardiovascular system, such as an increased risk of blood clotting.
- The vaccine-induced spike protein and its S1 subunit have been found in the blood following vaccination.
- In lab studies, the spike protein activates white blood cells and may trigger an inflammatory response or clotting.
- Free spike protein was found in the blood of adolescents and young adults with post-mRNA vaccine myocarditis but not in healthy control subjects without myocarditis.
- The S1 subunit can interact with ACE2, platelets, and fibrin and may be what leads to an inflammatory response driving serious adverse events, including clots, myocarditis, and neurological problems.
- As discussed in Part 3, lipid nanoparticles (LNPs) act as adjuvants, stimulating the immune system. This innate immune response peaks within six hours of vaccination and returns to baseline by about day nine, temporally corresponding to the onset of myocarditis, which typically occurs within the first seven days following mRNA COVID-19 vaccination.
- Studies have not been done to evaluate how vaccination affects those who have already been infected with SARS-CoV-2.
- The spike protein was implicated in small vessel microclots during COVID-19 illness; thus, postvaccination cardiovascular effects should have been anticipated.
- The first deadline for FDA-mandated post-authorization safety studies has passed, yet to the best of our knowledge, the full report has not been made available to the public.
The spike protein protrudes from the SARS-CoV-2 virus like a crown of sticky handles. The job of the spike protein is to grab onto the ACE2 receptor so the virus can enter the cell. The ACE2 receptor is found in many human cells in the lungs, kidneys, gut, heart, and the lining of the blood vessels.
Spike protein is comprised of two parts: the S1 and S2 subunits. The S1 subunit protein sits at the tip of the spike protein and is responsible for attaching to the ACE2 receptor. Once bound to the receptor, the spike protein changes shape to allow the virus to enter. Having accessed the inside of the cell, the SARS-CoV-2 virus uses the cell’s own protein manufacturing process to make new viral proteins.
Effective vaccines select recognizable antigens that induce a robust immune response. The spike protein was chosen for the mRNA COVID-19 vaccine because it is responsible for attaching to cells and gaining entry. However, research suggests that the spike protein and its S1 subunit may also be responsible for cardiovascular complications following both infection and vaccination.
The S2 subunit may also interfere with tumor suppression, potentially explaining why COVID-19 can be more severe for cancer patients.
Blood Clots Associated With Spike S1 Subunit
In laboratory experiments like those performed in the Frontiers in Immunology study, the spike protein S1 subunit causes a chain reaction that sets up the right conditions for clots to form. In this chain reaction, the S1 protein binds to the ACE2 receptor on the cells lining the blood vessels. Binding to ACE2 then activates immune cells.
This domino effect can also stimulate platelet binding, increasing clotting risk. Platelets are essential clotting agents that stop blood loss following injury by clumping together. The authors further noted that in vitro, “our group recently documented that exposing sera from severe COVID-19 patients to endothelial cells induced platelet aggregation.”
In other words, the S1 subunit is of interest because, in vitro (in a test tube), it appears to cause changes to clotting mechanisms. If the S1 subunit can affect clotting agents like fibrin, complement 3, and prothrombin, this may be a mechanism through which SARS-CoV-2 can cause cardiovascular complications. Clotting causes changes in blood flow, potentially leading to thrombosis, stroke, and heart attack.
Atypical Blood Clots
Providing blood thinners to decrease the risk of clot formation did not appear to reduce the clotting risk in COVID-19 inpatients or outpatients. This may be because the clots formed after exposure to the S1 subunit may not be typical blood clots. Three findings suggest that the S1 subunit is important to clotting risk.
1. Clots Resist Normal Breakdown
First, when the S1 subunit was added to healthy blood in the lab, it created dense, fibrous clot deposits. These fibrous “amyloid” clots formed even when blood taken from healthy people was exposed to the S1 subunit.
The S1 subunit appears to be associated with clotting resistant to fibrinolysis—the normal breakdown of clots necessary to restore blood flow after injury. These amyloid clots are shown in Figure 1 below.
Amyloid clots occur when a protein is damaged and begins to fold abnormally on itself. When these abnormal amyloid proteins accumulate in the body, they can interfere with normal function.
Figure 1. Amyloid Clots Formed in Response to Spike Protein S1
2. S1 Subunit Can Induce Amyloid Substances
Second, these dense clots may be caused by certain protein segments on the S1 subunit. The spike protein has seven protein segments (peptides) that can induce fibrous (amyloid) substances. While the fully intact spike protein (S1 and S2 subunits attached to form the full spike) did not form this amyloid, the S1 subunit did. This finding is interesting because it suggests that the subunits of the spike protein may have unique effects on cells.
