Diseases From SARS-CoV-2 Autoantibodies

This article features a study showing that autoimmune antibody production is greater among older people with severe COVID-19 infection. The study’s findings can help explain the adverse effects of the COVID “vaccines.”

Autoantibodies are antibodies that attack the host’s organs to cause inflammation that manifests as autoimmune diseases.

The paper is authored by several well-known institutions globally, including Brazil, the USA, Israel, and Germany.

The investigators studied 159 individuals with COVID-19 (71 milds, 61 moderate, and 27 severe patients) and 73 healthy controls.

The following antibodies that they found in severe COVID-19 patients are

1. Amyloid β peptide
2. β catenin
3. Cardiolipin
4. Claudin
5. Enteric nerve
6. Fibulin
7. Insulin receptor a
8. Platelet glycoprotein

Typically, antibodies are directed against foreign antigens like germs and viruses.

The Pfizer BNT162b2 and Moderna COVID shots contain the mRNA sequence to produce to spike protein of the SARS-CoV-2. The spike protein is the most toxic part of the virus and induces molecular mimicry to result in autoantibodies.

13 ways that the SARS-CoV-2 spike protein causes damage

Molecular mimicry is when the protein sequences in a foreign protein, like the spike protein, share similarities with the cells in the human body. Thus, any antibody formed against a segment of the spike protein that mimics a protein in human cells can be attacked by an autoantibody.

The spike protein has about a thousand amino acids. An antibody can form against five to seven amino acids. Just imagine or do the math on how many different types of antibodies can be produced against the spike protein.

In this part, I present the autoimmune diseases that may arise from autoantibodies. If you are closely following the COVID shots complications, you will find many familiar conditions below.

Amyloid βeta peptide

Amyloid beta is a neurotoxic protein found in the brains of patients with Alzheimer’s dementia. Being neurotoxic, it was first thought that antibodies to the Amyloid beta would be suitable.

As it turned out, the antibodies to the amyloid beta protein worsened the neurotoxicity of the amyloid beta protein and resulted in the brain cells degeneration.[2]

This mechanism explains why COVID-19 results in the worsening of Alzheimer’s disease. I discussed a separate means of why SARS-CoV-2 can worsen dementia in Similarities in the brain of SARS-CoV-2 and Alzheimer’s disease individuals and Mental and Neurologic problems after COVID-19 in children and adults.

Beta Catenin

Beta-catenin is a multi-tasking molecule that has a role in cell development and keeping cells in order. Any problem in its structure and signaling can lead to the deregulation of cell growth in cancer and metastasis. [3]

Currently, there is an explosion of cancer cases. A study published in Nature and an article in Cancer and Careers show a rise in cancer for 2022. Dr. Ryan Cole, a Mayo Clinic-trained pathologist,  has many interviews about it. You can listen to one HERE.

Cardiolipin

Cardiolipin was initially isolated in beef hearts, which is why “cardio” is in the name. Since then, it has been found in animal and plant cells and is a component of the inner membrane of the mitochondria.

Antibodies to cardiolipin result in anti-cardiolipin syndrome and blood clot formation like Deep Venous Thrombosis, Pulmonary Embolism, and arterial clots.

A pulmonary embolism is a blood clot in the lung that can kill someone suddenly or if they are left untreated. Arterial clots in the legs can lead to loss of blood supply and limb amputation.

An example is a 20-year-old who got her leg amputated after receiving a COVID shot and later died from blood clots in the brain.

Four ways the spike protein rapidly forms blood clots resistant to breakdown

Claudin

Claudin proteins are essential to maintain tight junctions between cells. A disruption of claudin is implicated in cancer formation.[4]

Antibodies to claudin and beta-catenin are probably instrumental in the rising number of cancer cases, as mentioned earlier.

Enteric nerve

Enteric nerves are found in the intestines. Anti-enteric antibodies have been found in Irritable Bowel syndrome.[5]

The symptoms of Irritable Bowel Syndrome are abnormal defecation associated with abdominal pain, both of which may be exacerbated by psychogenic stress.

Gastrointestinal complaints are some of the symptoms of Long COVID, as described in this Mayo Clinic article. Anti-enteric antibodies may play a significant role.

Fibulin

Fibulin is found in the blood and the extracellular matrices. The extracellular matrix is a three-dimensional network consisting of macromolecules and minerals that provide structural and biochemical support to surrounding cells.

One type of fibulin, Fibulin-5, is abundantly expressed in many tissues, including the aorta, lung, uterus, and skin, all of which contain abundant elastic fibers[6]

Any antibodies directed against any of the tissues with fibulin can cause inflammation in those organs.

Insulin receptor A

Insulin receptor antibodies are a rare or underreported cause of insulin resistance. Patients usually have a combination of high blood sugar, insulin resistance, acanthosis nigricans, and autoimmune features.

In one case report, a patient with antibodies to insulin receptors (not from COVID-19) was resistant to insulin therapy and required doses of up to 154,075 units daily. Typically, patients will only need less than 100 units of insulin daily in the hospital. The patient got better with steroids that stopped the antibodies. [7]

The anti-insulin receptor antibody can explain why severe COVID patients have high blood sugar, new-onset diabetes,[8] and hard-to-control diabetes. [9]

It can also happen after the COVID jabs. A case series described three patients who developed diabetic ketoacidosis and/or hyperosmolar hyperglycemic syndrome and new-onset diabetes mellitus (DM) within 2 to 10 days of the COVID-19 vaccination. [10]

Platelet glycoprotein

Platelet glycoproteins are found in the platelets that initiate blood clotting. Antibodies to platelet glycoproteins cause the platelets to stick together and are ineffective for clotting. This can lead to immune thrombocytopenia and bleeding. 

Antibodies to the platelet glycoprotein and cardiolipin explain why patients with severe COVID-19 have excessive blood clotting and bleeding simultaneously.

In their analysis, Fonseca et al. found that anti-cardiolipin and anti-platelet glycoprotein autoantibodies indicated a significantly increased likelihood of developing severe COVID-19. The authors conclude,

These findings provide new key insights to explain why elderly patients less favorable outcomes have than young individuals, suggesting new associations of distinct autoantibody levels with disease severity.

Conclusion

The featured study by Fonseca et al. explains why severe COVID-19 happens more in the elderly. It also provides a mechanistic explanation of why many adverse events occur after the COVID shots.

To know more about molecular mimicry with the SARS-CoV-2, look at the articles I wrote soon after the COVID injections were emergency-authorized.

1. COVID-19, Autoimmunity and Vaccination, Part 1
2. COVID-19, Autoimmunity, and Vaccination Part 2
3. COVID-19, Autoimmunity, and Vaccination Part 3
4. Molecular Mimicry between the SARS-CoV-2 and the Breathing Center
5. Molecular mimicry between the spike protein and humans can shut down platelet production
6. Autoimmune antibodies and diseases after COVID-19 disease and injections
7. The SARS-CoV-2 spike protein cross-reacts with eleven human proteins to cause autoimmune diseases

There are many articles about the pathophysiology of the adverse effects of COVID injections in my The Updated List of Covid-19 Articles 

Truth heals. Lies kill. Don’t Get Sick!

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