Posted on 01/07/2023 11:08:08 PM PST by libh8er
Introduction
The development of myocarditis following mRNA vaccination is rare, occurring in < 2 per 100,000 individuals. It remains an unpredictable mysterious occurrence. Some have suggested that it is linked to the overproduction of antibodies or abnormal immune responses.
Autoantibody production due to polyclonal B cell activation and proliferation has also been suggested, as has immune complex formation and inflammation. Finally, some think that cardiac antigens closely resembling the spike protein are targeted by autoantibodies formed as a result of molecular mimicry.
The immune response to these vaccines in these patients needs to be better understood in order to determine why and how it happens. It is imperative to study the role of male hormones since young male patients are most often affected.
The researchers in this study looked at blood samples from 16 myocarditis patients, confirmed to have high levels of serum cardiac troponin T. All developed myocarditis after receiving the COVID-19 vaccine, typically within a week of the second dose. However, a few became sick after the first dose or booster dose. Over 80% were male.
They were studied by antibody profiling, including antibodies to the virus, autoantibodies or antibodies to the virome, and the analysis of T cells specifically directed against the virus. In addition, cytokine and antigen profiles were determined. These measurements were compared with those of 45 vaccinated controls, who were of similar age and health.
What did the study show? All subjects and controls showed a rise in anti-spike antibodies and antibodies to the receptor binding domain (RBD), of all immunoglobulin (Ig) subclasses, IgA, IgM, and IgG. Functional differences were not perceived either, with Fc effector functions being similar in both categories. In short, all vaccinated individuals showed evidence of a protective immune response against the virus.
“We found no indication that a specific antibody response is associated with myocarditis.”
Additionally, these patients did not show evidence of increased autoantibody production or antibody production against other respiratory pathogens that differed in magnitude or range from the controls.
T cells of all relevant subtypes, including naïve, memory, and effector memory T cells, showed similar distributions in both groups. T cells also showed similar proportions of spike-specific memory CD4 T cells and activated CD4 and CD8 T cells. The only exceptions were the observation of small elevations in effector memory cells and PD-1-expressing bulk CD4 T cells in the myocarditis group.
The findings indicated that antibody and T-cell responses could not distinguish between post-vaccine myocarditis subjects and vaccinated controls. The only significant difference was a slight elevation in cytokine production in the former.
The exciting difference was the high level of circulating full-length spike protein in the plasma of myocarditis patients, at a mean of ~34 pg/mL. Furthermore, the protein was not bound to antibodies and remained detectable for up to three weeks from the vaccination date. In contrast, controls did not have free spike protein in their blood.
This difference could not be attributed to poor neutralizing capacity in the myocarditis group, which showed comparable neutralization relative to the control group.
Concordantly, myocarditis patients had cytokine release patterns resembling those found in multisystem inflammatory syndrome in children (MIS-C). This might indicate that the innate immune response was overactive, leading to elevations in interleukin (IL)-8, IL-10, IL-4, IL-6, tumor necrosis factor (TNF)-α, and interferon (INF)-γ relative to healthy controls. IL-8 was most closely associated with raised cardiac troponin T and antigen levels.
Alongside, leukocytes, especially neutrophils, were at higher mean levels in this group than controls, though still within normal range.
What are the implications? The study shows that the immunological response elicited by the mRNA vaccine was very similar in those who developed post-vaccination myocarditis and others. In other words, myocarditis could not be associated with abnormal autoantibodies, viral infections other than SARS-CoV-2, or excessive production of antibodies elicited by the mRNA vaccine.
In vaccinated patients, infection with the virus was not likely to be a cause or contributing factor for myocarditis since anti-Nucleoprotein IgG was not found in these patients.
In contrast to controls, the finding of high levels of unbound full-length spike protein in myocarditis patients may point to the mechanism by which this condition arises. Similarly, MIS-C patients had circulating SARS-CoV-2 antigens.
The spike protein appears to evade immune antibodies found at normal levels in these patients, with adequate functional and neutralization capacity. The spike may damage the cardiac pericytes or endothelium, perhaps by reducing the expression of the angiotensin-converting enzyme 2 (ACE2), reducing nitric oxide production in the endothelium, or activating inflammation via integrins, causing the endothelium to become abnormally permeable.
“Thus, the spike antigen itself, which evades antibody recognition rather than invoking immune hyperactivation, may contribute to myocarditis in these individuals.”
This finding does not amount to evidence against the benefit of vaccination with these vaccines, which effectively protect against severe COVID-19 outcomes. Therefore, current vaccine recommendations are unlikely to be altered due to these results.
“Understanding the immunopathological mechanisms associated with postvaccine myocarditis will help improve safety and guide the development of future coronavirus disease 2019 (COVID-19) vaccines. These findings also suggest that administration of anti-spike antibodies, if spike antigenemia is detected, could potentially prevent or reverse postvaccine myocarditis.”
BULL HOCKEY!
Fauxi said in Jan 2020 that masks don't stop respiratory viruses and this is just a bad flu.
The last time (the only time) he told the truth.
Actually, he was lying then, too.
My January 2020 chest xrays showed clean, clear lungs.
In February and March of 2020, I was hospitalized with breathing issues.
In April of 2020, a pulmonologist confirmed COVID scarring all over my lungs.
Got COVID again over the summer. Pulmonologist puts me at Stage 2 COPD.
I was thin, healthy, and only 54. As quickly as it is progressing, I have only a few years left to live.
So no, it was not the flu. I had the flu in the past and bounced right back.
Fauci’s monster is a death sentence for me.
Quite different from what Dr. McCullough recently found, that myocarditis was being reported in 1 in 40 vaccinated ppl. I wonder who funded this study using 16 patients from Massachusetts General Hospital. The article says funding info can be found on page XXX, but naturally I can’t access that info without a subscription to the “Circulation” publication.
I’m so sorry to hear this. I’ll pray for your healing.
This is a good article.
“This might indicate that the innate immune response was overactive”
RNA activates the innate immune system.
The presence of the spike protein in myocarditis is interesting. It does indicate the mRNA is still present also.
The problem with the mRNA spike protein technology is people do not understand it. To be brief, that protein never gets loose in the bloodstream.
“The article says funding info can be found on page XXX, but naturally I can’t access that info without a subscription to the “Circulation” publication”.
It is accessible without subscription.
https://www.ahajournals.org/doi/epdf/10.1161/CIRCULATIONAHA.122.061025
Look at page 9.
The problem with the COVID virus is it rapidly reproduces as it hijacks to reproductive mechanism of the cell. The immune system that is primed by the vaccine has to catch up to the spreading virus in the body. By the time it gets the virus under control, the virus has already shed through the lungs to infect others. The U.S. Government did a lousy job educating the public. I think it was criminal.
1. Is there a way to detect possibility of myocarditis?
2. Are there mitigation strategies against myocarditis if it is known/unknown?
Last on the funding list - Gates Foundation Global Health Vaccine Accelerator Platform funding (OPP1146996 and INV-001650).
What a surprise..................NOT!!!
+1
ping
I just went through this. They may be able to see swelling on xrays. The best way is an angioplasty (mine was done on Thursday; thankfully, no myocarditis).
Depending on what stage it is detected, you can survive. Late stage myocarditis kills 70% of people within 5 years.
I was not vaxxed.
Most people aren’t aware that you can get myocarditis from COVID. Given the damage it did to my lungs, and the symptoms I was experiencing, COVID-related myocarditis seemed a likely culprit. I was fortunate that my heart is in good shape.
Next stop, the neurologist.
On a serious note, whenever something new (like the mRNA vacc.), barely understood, and not tested over time is introduced into a huge percentage of the population, things are bound to go wrong.
may, might, perhaps
If you think we're going to build a case where ANYONE is liable...you're kidding yourself...you don't bite the hand that feeds you...Isn't that right Dr. Fauci??
Even the corrupt government admitted the spike protein enters the bloodstream back in 2021.
https://pubmed.ncbi.nlm.nih.gov/36597886/
"Conclusions: ...However, free spike antigen was detected in the blood of adolescents and young adults who developed post-mRNA vaccine myocarditis, advancing insight into its potential underlying cause. "
So now myocarditis goes from ‘impossible’, to ‘extremely rare’. When will the whole truth be allowed to be printed?
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