Exploring Spike Protein’s Impact on Myocarditis & Blood Clotting Post COVID-19 Vaccination

In this ‍series, “Promise or Peril: Alarming COVID-19 mRNA Vaccine Issues,” we ⁤explore how ‍the​ introduction of mRNA technology lacked an adequate regulatory framework, setting the stage ‍for serious adverse events ⁣and other concerns related⁤ to inadequate safety testing of lipid ⁢nanoparticles, spike⁢ protein, and residual DNA- and lipid-related impurities, as well as truncated/modified mRNA species.

Previously: ​In ‍Part 1, we introduced how the U.S. Food ⁢and Drug Administration (FDA) relaxed the rules ⁤for ⁤mRNA ⁣vaccines compared⁤ to mRNA therapies and discussed the available data regarding LNP distribution throughout the body based ​on ​animal⁢ testing, the fact that‍ human testing was not done, and the ⁣lack of mRNA or spike protein biodistribution‌ data. In Parts 2 and⁤ 3, we explored how the LNPs are constructed and how they behave ​in⁤ the body and affect⁣ health.

Health Viewpoints

Now we turn to another problem—the cargo contained in‍ the LNP​ capsules: the mRNA‍ and its encoded spike ⁣protein. We introduce the inflammatory response to the ​spike protein and one of its subunit proteins and how they may contribute to serious adverse ​events such as‌ myocarditis and blood clotting.

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.

Research shows that the spike protein is found in the⁤ blood following COVID-19 infection and vaccination.‌ The spike protein modifies blood clotting and ​can stimulate an overactive‌ immune response. A ⁣better understanding of ‍these findings and the specific roles the ⁢spike protein ⁢and its ⁢S1 subunit⁢ play will help us determine who is ⁢most at risk‌ for severe disease or vaccine adverse events.

Cardiovascular ⁤Effects of ‍Spike Protein Following Infection

Although ⁢the studies are ​small,‍ the spike protein has been found in the blood and clots ‌of severely ill COVID-19 patients. The clinical evidence suggests a fingerprint of the spike protein’s cardiovascular effects.

In a study of⁢ 41 patients⁣ published in Frontiers in Immunology, 30.4‌ percent ​of the 23 hospitalized were found to have significant levels of spike protein in their circulation. None​ of the‍ remaining 18 uninfected or mildly ill individuals had circulating spike protein.

A⁣ small case-control study detected the⁤ spike protein in clots retrieved ⁣from COVID-19 patients with acute ischemic stroke ⁣and myocardial ​infarction.

Another study detected⁢ the S1 subunit in the plasma‍ of 64 percent of COVID-19-positive patients, and S1 levels were ‌significantly associated ⁣with disease severity. The nucleocapsid (N) protein, a marker for COVID-19 infection, was ​also ‌detected. ⁣The authors speculated that the presence of S1 and ⁣N ⁢in plasma suggests⁣ that virus​ fragments‌ enter the bloodstream, potentially⁤ due to tissue damage.

The exact chain of​ events is not fully understood. Still, laboratory, clinical, and biopsy findings offer converging ‌evidence suggesting a role for ⁣the spike protein and ⁢its⁢ S1⁣ subunit⁤ in blood clotting⁣ and heart injury.

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.

3. Spike Blocks Other Clot-Inhibiting Proteins

Third, ⁢spike ⁢protein can ‌outcompete ‌other‍ proteins,⁤ which ‌prevent clots from ‌forming. In another⁢ laboratory experiment designed to understand ⁣how this process plays ⁤out, scientists found that the‍ spike protein blocks ​proteins important⁣ to breaking down clots.

In summary, the in vitro (laboratory-based) research suggests that the spike protein subunit S1 can‍ induce clot formation and impair clot ‌dissolution. ‌While we do not know precisely how this translates to⁣ processes in the body, Epoch Times’ Jan​ Jekielek explored clotting and the ‌role of spike⁤ protein with pathologist Dr. Ryan Cole on June‌ 3 ⁤ and Dr. Paul Marik on May 23. In the interview, Dr. Cole explained‍ that the spike​ protein ⁣persists in the body longer, inflames‍ tissues wherever‍ it lands, and acts as an irritant ⁤or toxin in the body.

Spike Protein⁤ Found in COVID-19-Vaccinated Myocarditis Patients

Studies of COVID-19-vaccinated patients diagnosed with myocarditis found spike protein in the patients’ blood and heart muscles ​but not in those without myocarditis.

Found in Blood

The full-length spike⁢ protein has been found in the blood of⁢ vaccinated ​adolescents with myocarditis but ‍not in⁣ the blood of those without myocarditis.

It‍ is unclear why the ⁢spike protein was circulating ⁤freely⁤ or unbound by antibodies. The adolescents who developed myocarditis‌ had similar immune markers ​to those who did not develop myocarditis. In‌ other​ words, the group with myocarditis did not​ appear to‍ have any immune problems.

Rather, ⁣these adolescents may have had⁤ an overactive natural immune response. Strong natural ⁤(“innate”) immunity ⁣helps the ⁢body fight off disease without any ⁢prior exposure. However,‍ the first​ responders (inflammatory cytokines) ⁢can sometimes⁣ be exuberant. ‌If ​the innate immune response overreacts, it may trigger myocarditis.

Found in Heart ​Muscle

The spike protein coded by mRNA ‌has also been​ found‌ in heart ⁣muscle cells. ⁤An ⁤endomyocardial (heart muscle) biopsy study ⁤ was⁤ conducted among 15 patients‍ with myocarditis⁢ following ⁣vaccination. No other viral infection could be found that might have caused the myocarditis.

The investigators found SARS-CoV-2 spike protein in nine of the ⁣15 patients. Immune cells (CD4+ T) ​were ⁢also detected in ‍the ⁤biopsy samples.⁣ These observations suggest an ⁣inflammatory reaction ​to​ the spike protein.

The authors concluded: “Although a⁤ causal relationship between vaccination and the occurrence of myocardial inflammation cannot be established⁣ based on the findings, the cardiac detection of‌ spike⁤ protein, the CD4+ ⁣T-cell-dominated inflammation, and the close‌ temporal relationship argue for a vaccine-triggered autoimmune reaction.”

A 2022 modeling study also suggests that⁤ the spike protein can‌ cause an autoimmune⁤ response by mimicking human⁣ molecules, causing antibodies to bind​ to “self” proteins.

Spike S1 Detected in the Blood​ of Vaccinated‌ Adults

Another study found‌ that 11 of ‌13 adults vaccinated with Moderna’s mRNA-1273 had the ‌ S1 subunit in their blood as early as one day after‌ vaccination.

Plasma was‌ collected from 13 participants at various times during the first month after each dose. The antigens S1 and spike were measured to estimate the amount of mRNA translation into ⁣protein products.

After the first 100-microgram dose, S1 antigen was detected in the ‌plasma ⁢of 11 participants. In contrast, the spike antigen ‍was detected in ‍three of 13 participants. The S1 antigen peak was detected on average five days after vaccination. ⁣Again, the timing of this peak for S1 seems to add to the clues​ suggesting an autoimmune ⁣response in the week after vaccination.

mRNA Detected in the Blood and Lymph Nodes After ‌Vaccination

Vaccine mRNA, which encodes the spike protein and its S1 subunit, also ⁣persists in the blood and lymph nodes. Following vaccination, spike-encoded mRNA has been found in the blood for 15 days and ⁢in lymph nodes for up to 60 days. Spike-laden exosomes ​ have been found circulating in ⁢the blood for up to four months. This finding is important because it refutes‍ the CDC’s claim ⁤that ‍the mRNA is so fragile that it dissolves quickly at the injection site (see​ Figure 2a⁣ in Part 1).

The lymph nodes continue creating better-fitting antibodies after any viral infection. This‌ is a critical way that our bodies⁤ prepare for new variants naturally. ​However, persistently high levels‍ of vaccine-induced mRNA and spike ⁢protein⁤ may not‌ be helpful‌ when the immune system ​is asked to respond to future variants. In ⁣other words, if the ‌immune system is tasked with​ continuing to pump⁤ out antibodies to​ a ‍previous⁣ variant,‌ it⁢ may be ⁢less nimble when asked to ⁣create a high-quality antibody for a new variant.

Inadequate Clinical Trials Leave Unresolved Questions

Given what we ‍know about ‍the harmful effects of⁤ the SARS-CoV-2 virus, we should not have⁤ assumed ⁣that⁢ the vaccine-encoded spike⁤ protein would be harmless.

And, given what we know about ⁣clotting issues following COVID-19 infection, future studies should‍ test whether the S1 subunit produced in response​ to vaccination⁢ can ⁤also ⁤cause clotting issues via the same pathway. These studies should ‍include both lab experiments and human observations.

In addition,⁣ we do not know the relative amounts of free spike protein​ in circulation following infection ‌versus vaccination.

In the case of the COVID-19 vaccines, the active ingredient was‍ not studied prior to authorization. The manufacturers used mRNA that encodes for a substitute⁣ protein (luciferase) to test the safety and biodistribution of the mRNA vaccines.

Pfizer submitted animal biodistribution data to‍ regulatory agencies using ⁤the surrogate ⁣RNA encoding for luciferase, as discussed in Part 1 of this series.

However, these studies were inadequate⁣ in describing how mRNA, the ⁤spike protein, its S1 subunit, and the⁣ LNP carrier ⁣would affect the human body.

In this article, we described laboratory findings showing clotting associated with the S1 subunit. Studies‍ like these reinforce why thorough‍ preclinical studies are so ⁤crucial. The studies conducted by pharmaceutical companies were‍ not sufficient⁤ to ⁤address these questions.

We had very little information about how people would respond to vaccination depending on age, sex, immune ‌status, ⁤overall health,⁣ or history of prior‍ SARS-CoV-2 infection. The⁣ original clinical trials did not ⁣enroll enough people who had already ⁤recovered from COVID-19; they ⁣were not designed to provide an‌ understanding of how ⁤prior infection would affect a person’s⁢ response to vaccination.

Required Pfizer Post-Authorization Safety Study ‌Unavailable to Public

Pre-authorization studies were clearly ​inadequate. Post-authorization, the FDA has only acknowledged that passive⁤ surveillance is insufficient to establish‌ safety. The agency responded to adverse event reports by ‍requiring Pfizer to conduct additional studies, with the first monitoring report ⁤due October 2022.

On page 6 of the approval letter, the FDA acknowledges ​this fact (see Figure 2 below):

“We‍ have determined that an analysis‍ of ⁤spontaneous ​postmarketing adverse events reported under section 505(k)(1) of the FDCA will ⁢not be‍ sufficient to assess ⁤known serious⁢ risks of‌ myocarditis and pericarditis and identify an unexpected serious risk of subclinical myocarditis.

“Furthermore, the pharmacovigilance system that the⁤ FDA‍ is required to ⁢maintain under section ⁤505(k)(3) of the FDCA is‌ not sufficient to assess these serious risks. Therefore,​ based on appropriate scientific data,⁢ we have ‌determined ⁣that you are required to conduct the following studies. …”

Has the FDA ⁢received the monitoring ​report ‍from Pfizer, which was due by Oct. ⁤31, 2022? The next report, the interim report, will be due in October.

Figure 2.‍ FDA Postmarketing Safety Study Requirements

Read ‌Part ⁤1: FDA Overhaul Needed for New ⁢Vaccines and mRNA Therapies

Read Part 2:Health Implications of Poor COVID-19 mRNA ​Testing: Miscarriage, Vision Loss,‍ Immunotoxicity

Read Part ⁤3: Pulling Back the Curtain: mRNA Lipid Nanoparticle Design Created Potential ⁤for Clotting and Triggering Immune Overdrive

Next: In Part 5, we will discuss the⁤ mRNA manufacturing issues affecting ⁤contamination with ‍double-stranded DNA and ‌the ⁣potential for⁢ genome integration.

◊ References

Addgene. Molecular Biology Reference. https://www.addgene.org/mol-bio-reference/#introduction

Alana F Ogata, Chi-An Cheng, Michaël Desjardins, ⁤Yasmeen Senussi, Amy C Sherman, Megan Powell, Lewis Novack, Salena Von, Xiaofang Li,‌ Lindsey⁢ R Baden, David R Walt, Circulating Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Vaccine‍ Antigen Detected in the ‌Plasma of ⁢mRNA-1273 Vaccine Recipients, Clinical Infectious Diseases, Volume 74, Issue 4, 15 February 2022, Pages 715–718, https://doi.org/10.1093/cid/ciab465

Aldén M, Olofsson Falla F, Yang D, Barghouth M, Luan⁤ C, Rasmussen M, De Marinis​ Y. Intracellular Reverse Transcription of Pfizer BioNTech ​COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line. Curr Issues Mol Biol. 2022 Feb⁤ 25;44(3):1115-1126. doi: 10.3390/cimb44030073. PMID: 35723296; ‍PMCID: PMC8946961. https://pubmed.ncbi.nlm.nih.gov/35723296/

Allergic Reactions Including Anaphylaxis ​After Receipt ⁢of the First Dose of Pfizer-BioNTech COVID-19 Vaccine — United States, ‌December 14–23, 2020. MMWR Morb Mortal Wkly​ Rep 2021;70:46–51. DOI: http://dx.doi.org/10.15585/mmwr.mm7002e1

Anderson ⁤EJ, Rouphael NG, Widge AT, et al. ⁤Safety and Immunogenicity ‌of SARS-CoV-2 mRNA-1273 Vaccine in ⁤Older Adults N Engl J Med 2020; 383:2427-2438 https://www.nejm.org/doi/full/10.1056/NEJMoa2028436

Anderson ⁤S. CBER Plans for Monitoring COVID-19‍ Vaccine Safety and Effectiveness. https://stacks.cdc.gov/view/cdc/97349 ⁢October ⁢20, 2020. Accessed 3/20/23.

Angeli F, Spanevello A, Reboldi G, Visca D, Verdecchia P. SARS-CoV-2 vaccines: Lights and shadows. Eur J Intern Med. 2021‍ Jun;88:1-8. doi: 10.1016/j.ejim.2021.04.019. Epub 2021 Apr 30. PMID: 33966930; PMCID: PMC8084611.⁢ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084611/#bib0043

Baker, A. T., Boyd,‌ R. J., Sarkar, D., Teijeira-Crespo, ‍A., ⁢Chan, C. K., Bates, E., Waraich,⁣ K.,​ Vant, J., Wilson, E., Truong, C. D.,⁤ Lipka-Lloyd, M., Fromme, P., Vermaas,​ J., Williams, D., Machiesky, L., Heurich, M., Nagalo, B. M.,‌ Coughlan, L., Umlauf, S., Chiu, P. L., … Borad, M. J. (2021). ChAdOx1 interacts with⁤ CAR and PF4 with implications for thrombosis with‌ thrombocytopenia syndrome. ⁢Science Advances. ‌7(49), eabl8213. https://doi.org/10.1126/sciadv.abl8213

Baumeier C, Aleshcheva G,⁣ Harms D, Gross U, Hamm C,​ Assmus⁢ B, ⁤Westenfeld R, Kelm M, ⁢Rammos S,​ Wenzel P, Münzel T, Elsässer A, Gailani M, Perings C, Bourakkadi⁣ A, Flesch M, Kempf