Can these shots cause autoimmune disease?
Autoimmunity is an immune response in an organism against its own healthy cells, and any disease resulting from this type of immune response is called an “autoimmune disease”.
To make myself more clear, autoimmunity isn’t all ‘bad’ per se and in fact, occurs in all individuals. Low levels of autoimmunity help with the selection of white blood cells, helps balance and prepare the immune system, and also help protect the body against organ damage.
Although autoimmune immune cells exist in all healthy individuals, a relatively small portion of the population develops autoimmune diseases. This is due to the tight regulation of the immune system becoming untangled, as well as other factors like differences in underlying genetics and pathogen exposure.
In those with autoimmune disease, immunological tolerance - the ability to ignore “self”, while reacting to “non-self” antigens - becomes broken. This breakage leads to an unending attack of one’s own body by one’s own immune system.
One mediator of immunological tolerance are regulatory T (Treg) cells. Treg cells help modulate helper T-cell activity and restrict fulminant autoimmunity. And so, as you have guessed, numerical or functional Treg defects are linked to autoimmunity.
Another way autoimmunity may be triggered is via a mechanism called “molecular mimicry”. Here, antigens that aren’t made in the body share structural similarities with antigens found naturally within the body. And thus antibodies formed to bind to the former, and also bind to the latter. It is thought that molecular mimicry is a pervasive strategy employed by viruses to harness or disrupt host cellular functions.
One of the first experiments to identify molecular mimicry was carried out in 1983 and found that murine antibodies to measles virus and herpes simplex virus (HSV) were found to react against human cells.
Since then many other studies have cemented the link between molecular mimicry and autoimmunity. Vaccines too haven’t gotten off scot-free.
The influenza A vaccine has been linked to narcolepsy and Guillain-Barré syndrome (a neurological condition causing muscle weakness and paralysis); the hepatitis B vaccine to a 5-fold increased risk of multiple sclerosis; and the human papillomaviruses (HPV) vaccines to postural orthostatic tachycardia syndromes (POTS - a disorder of the autonomic nervous system characterised by heart rate changes linked to changes in posture). All of this has been postulated to be down to molecular mimicry.
Those prone to autoimmune diseases also commonly show a dysfunction with their CD8+ ‘’killer (or cytotoxic) T cells’’. In a normal infection, a productive CD8+ T cell response is generated, the pathogen is cleared and immunological memory is formed. Job done.
By comparison, when there is chronic antigen stimulation - in the context of conditions like cancer, long-term infections and autoimmunity - CD8+ T cells either become ‘exhausted’ or exhibit excessive and inappropriate autoimmunity causing self-damage. This dysfunction in turn contributes to viral persistence and continued tumour growth.
We now know that certain traditional vaccines can increase one's risk of certain autoimmune diseases. But what about mRNA jabs? To understand the risk of developing autoimmune disease after the shots, we’ve got to first really understand the mechanism by which they work.
See, traditional vaccines consist of inactivated or weakened viruses which in turn allows the immune system to mount a response and form immunological memory without causing an infection.
mRNA jabs on the other hand train regular human cells to make and then present SARS-CoV-2 spike protein on its surface. These cells are identified by the immune system and destroyed. An autoimmune reaction.
The whole immunological basis of these mRNA jabs relies on autoimmune reactions. This comes to no surprise as one must remember that mRNA technology was originally made to stimulate T cells to destroy tumour cells.
With regard to molecular mimicry, it isn’t looking hopeful either. One study noted that “SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues.”.
Another study noted cross-reactivity between an antibody with affinity for Spike protein and a human protein, and note, “consideration of cross-reactivity for SARS-CoV-2 is important for therapeutic intervention and when designing the next generation of COVID-19 vaccines to avoid potential autoimmune interference.”.
And the evidence of molecular mimicry between SARS-CoV-2 proteins and our own continues to mount. Here are some extracts from recent studies on this topic:
“20 novel human peptides mimicked by SARS-CoV-2 have not been observed in any previous coronavirus strains”
“We report that SARS-CoV-2 has evolved a unique S1/S2 cleavage site, absent in any previous coronavirus sequenced, resulting in the striking mimicry of an identical FURIN-cleavable peptide on the human epithelial sodium channel α-subunit (ENaC-α)”
“we find that, relative to their proteome size, single-stranded RNA (ssRNA) viruses, including coronaviruses (CoVs), have circumvented the limitations of their small genomes by mimicking human proteins to a greater extent than their large dsDNA counterparts like Pox and Herpes viruses”
“COVID-19 induces a marked humoral response against the major protein of high-density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long-term COVID-19 prognosis assessment and warrant further scrutiny in the current COVID-19 pandemic.”
“.. identified previously known autoreactivities, and also detected undescribed neutralizing interferon lambda 3 (IFN-λ3) autoantibodies.”
“It would be expected that the COVID-19 pandemic and the vaccination against this pathogen could significantly increase the ADs incidences, especially in populations harboring HLA-B*08:01, HLA-A*024:02, HLA-A*11:01 and HLA-B*27:05. The Southeast Asia, East Asia, and Oceania are at higher risk of AD development.”
“This immune survey reveals evidence of a compartmentalized immune response in the CNS of individuals with COVID-19 and suggests a role of autoimmunity in neurologic sequelae of COVID-19.”
Aspects of autoimmunity have also been noted in those suffering from severe COVID-19. One study showed that those who suffered worse off had higher circulating levels of autoantibodies than those with a mild infection, highlighting the important point that not all antibodies are made equally. This was further reinstated in another study that noted that the majority of SARS-CoV-2-specific antibodies in COVID-19 patients with obesity were autoimmune and not neutralising.
Certain autoantibodies have also been related to clotting and bleeding disorders. And autopsies of Chinese citizens who died from COVID-19 showed evidence of lung scarring, again suggesting an autoimmune basis of COVID-19.
So do these shots cause autoimmune disease?
We know severely ill COVID-19 patients show impaired CD8+ T cell function and reduced levels of Treg cells. We know that traditional vaccines are linked to autoimmune diseases. We know that the basis of these mRNA jabs relies on autoimmune attacks. We know that the virus and its spike protein are structurally very similar to many human proteins. We know that high levels of autoantibodies correlate with disease severity.
So going by what we know so far theoretically, it would be unwise to answer that question with a simple “no”.
It would be further unwise (and plain wrong) to answer “no”, because we have real-life evidence that these shots do trigger autoimmune diseases, and sometimes fatally.
Vaccine-induced thrombotic thrombocytopenia (VITT) is a blood disorder that is characterised by widespread blood clots, predominantly in atypical sites like the brain and lungs, in combination with low platelet counts after receiving the COVID-19 shot.
Studies and VAERS reports have highlighted many cases of VITT, and the majority of people were previously healthy and with the absence of personal or family history of thromboembolic events. VITT has a mean time to onset of symptoms after inoculation of 8 days and predominantly affects females more of those aged 27 to 62 years old. Blood tests in those with VITT show elevated serum D-dimer, low fibrinogen level and positive PF4 antibodies.
To give you an idea of how serious VITT can be, I present to you one study that described in detail the clinical and laboratory profiles of 22 patients in which VITT developed.
“Among these 22 patients, 14 cases were women, with an age range of 21–77 years, and 21 had elevated D-dimer levels, positive PF4 antibodies and abnormal fibrinogen levels. In addition, 13 of these 22 patients had cerebral venous sinus thrombosis; four cases had a pulmonary embolism, one case had deep vein thrombosis and bilateral adrenal haemorrhage, two cases had ischaemic stroke affecting the middle cerebral artery region, and two cases had portal vein thrombosis.”.
Strokes, brain bleeds, and more. Autoimmunity is no joke. And other forms of autoimmune diseases have been described post-jab too.
Immune thrombocytopenic purpura (ITP) is an autoimmune condition characterised by a lowered platelet count which leads to inappropriate bleeding from various biological sites. Again many cases of ITP after COVID-19 jabs have been described in the literature.
The first case was of a 28-year-old male who presented to the Emergency Department around three weeks after his first dose of the AstraZeneca shot due to oral bleeding and the appearance of pinpoint bruising from broken capillaries (medically termed ‘petechiae’) over his body, arms, and legs for three days. The medical examination further revealed bleeding lesions in his mouth.
It is thought that ITP occurs due to pathogenic antibodies binding to platelets and to cells involved in the production of platelets called megakaryocytes, leading to reduced platelet counts through various immune pathways.
Autoimmune liver disease has also been reported post-jab repeatedly in the scientific literature. People present with deranged liver function blood tests and even jaundice. The mean time to onset of symptoms after inoculation is 13 days.
Guillain–Barré syndrome (GBS) is a rare autoimmune neurological disorder that affects the nerves causing limb weakness and changes in sensation. And again, it’s been repeatedly described in the literature after individuals have had these mRNA shots.
In addition to the complications described above, other autoimmune manifestations have been reported in some cases, such as
IgA nephropathy - a kidney disease that occurs when IgA deposits build up in the kidneys, causing inflammation that damages kidney tissues.
Inflammatory arthritis
Systemic lupus erythematosus - a widespread autoimmune condition causing systemic inflammation.
Graves’ disease - an autoimmune condition where your immune system mistakenly attacks your thyroid which causes it to become overactive.
It looks like those prone to autoimmune diseases may be at greater risk of said diseases post-jab. Remember too that autoimmunity requires chronic antigen stimulation. This may mean that those who have had more shots and/or COVID-19 infections are more likely to suffer from autoimmune diseases in the future.
Why are women more likely to suffer these sorts of side effects?
Women are more prone to autoimmunity in general, and this is looking like the case post-jab too. This is thought due to imbalanced X-chromosome inactivation and the involvement of female sex hormones.
Females have two X chromosomes, X-inactivation is where one of the copies of the X chromosome is inactivated. This is normal as X-inactivation prevents them from having twice as many X chromosome gene products as males.
Skewed X-chromosome inactivation, occurs when the X-inactivation of one X chromosome is favoured over the other. Some will have extreme skewing however and this is deemed medically important due to the increased potential for the expression of disease genes present on the X chromosome that are normally not expressed due to random X-inactivation.
And growing evidence suggests that this plays a part in certain autoimmune conditions, including autoimmune thyroid disease (ATD) and scleroderma.
So to conclude, can these shots cause autoimmune disease? Yes.
And the risk of these are greater if you’re female.
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