Note:
The SUMMARY was moved to the beginning of the article, which i always do. Some DETAILS were deleted to remove scientific details too complex for me to follow.
Ye Editor
"SUMMARY:
Changes to key parts of the mRNA code in SARS-CoV-2 vaccines may be causal in changing the innate immune response via toll-like receptors.
Toll-like receptors are important components in defence against infection, and downstream effects may also include inhibition of CD8 T cell response.
CD8 is a vital part of the immune system’s ability to eradicate infection and cancer.
Those changes may be reflected in recent reactivated Varicella Zoster (aka shingles) infections, although specific mechanisms are unclear at the moment.
Anecdotal reports of significant uptick in cancer presenting to medical consultants may be consistent with aberrant toll-like receptor and dendritic cell changes leading to an inhibition of the anti-cancer CD8 effector response.
Further data are required, but the prospect of an altered CD8 response to infection and cancer is very concerning and should prompt urgent investigation.
One might be forgiven for asking:
Surely someone must have cautioned against doing that?
And isn’t that why new drug / vaccine products are supposed to be thoroughly tested before they are given to large populations?
DETAILS:
"The fundamental change discovered by Weissman and Kariko was that nucleoside modification could protect mRNA from the body’s immune defences:
We show that RNA signals through human TLR3, TLR7, and TLR8, but incorporation of modified nucleosides m5C, m6A, m5U, s2U, or pseudouridine ablates activity.
Their key discovery here was that, by modifying the RNA code (modifying the nucleoside uridine), which would result in ablating the innate immune response, toll-like receptors (TLR) were necessarily involved.
This discovery was adopted in the mRNA technology used in Covid vaccines, in order that the foreign vaccine mRNA could enter cells without being destroyed.
... The body possesses two broad parts to its immune system: innate and specific.
The innate is the first to go into action against foreign invaders, including foreign mRNA from a vaccine.
How does that simple removal of one letter of code from mRNA achieve that?
It does so by affecting Toll Like Receptors (TLR): the alarm signal of the Innate Immune System.
The key TLRs affected are TLR 3, TLR 7 and TLR 8.
They act as sentries, whose job is to recognise foreign invaders by way of their form or patterns; a bit like an aircraft spotter in World War II.
If the wrong type of shape is recognised in the sky, then alarm bells sound and anti-aircraft fire kicks in. In the case of TLRs, the immune system gets activated.
What if you could by-pass those spotters?
No alarms, no immune system response; and your payload, foreign mRNA in this example, gets through safely.
Then your drug/vaccine has a much greater chance of working.
At that point in the original experiments – to discover how to turn off toll-like receptors (and subsequently in the design of the vaccines), the question should have been asked:
But what would be the consequences of switching off that important early warning system?
If that question was raised, it appears to have fallen on deaf ears and not been answered until, possibly, now.
Aberrant immune response
Dominguez-Andres et al addressed that question May 6th, 2021.
They state:
[C]ertain vaccines such as Bacillus Calmette-Guérin (BCG) and the measles, mumps, and rubella (MMR) vaccine also induce long term functional reprogramming of cells of the innate immune system.
(Netea et al., 2020).
This biological process is also termed trained immunity when it involves increased responsiveness, or innate immune tolerance when it is characterized by decreased cytokine production (Ifrim et al., 2014).
Although these effects have been proven mainly for live attenuated vaccines, we sought to investigate whether the BNT162b2 [Pfizer] vaccine might also induce effects on innate immune responses against different viral, bacterial and fungal stimuli.
Their answer?
[The] BNT162b2 (Pfizer) vaccine also modulated the production of inflammatory cytokines by innate immune cells upon stimulation with both specific (SARS-CoV-2) and non-specific (viral, fungal and bacterial) stimuli.
The response of innate immune cells to TLR4 and TLR7/8 ligands was lower after BNT162b2 vaccination.
They continue:
... These results collectively demonstrate that the effects of the BNT162b2 vaccine go beyond the adaptive immune system and can also modulate innate immune responses.
Three concerns are raised by the above.
The ability of the immune system to fight viruses has been diminished; specifically, the ability to fight SARS-CoV-2 may be affected;
Vaccine-induced innate immune tolerance may affect other vaccines;
and finally
What other parts of the immune system may be affected?
... On social media and online magazines we are now seeing reports of patients with worsening cancer following SARS-CoV-2 vaccination,
... In the articles above, any causal effect by the vaccine is quickly dismissed ...
(some people) are not convinced by the prevailing narrative and suspect that SARS-CoV-2 vaccination is contributing:
Dr Ryan Cole, a Pathologist, in a recent presentation, stated that he is observing a 20x uptick in endometrial cancer, and increases in other cancers post SARS-CoV-2 vaccination.
And even more concerning:
a senior consultant with decades of diagnosis and treatment at a dedicated cancer hospital described to a journalist off the record that all his vaccinated cancer patients were coming out of remission;
and that cancer was jumping between organs, spreading at a speed that he has never seen before (personal communication).
At this stage, these reports are anecdotal, but if they reflect a hitherto hidden change in the nature of how cancer is affecting patients post-vaccine, then what would be the mechanism?
And to what degree might it be obscured, even if just initially, by the expected increase in morbidity and mortality as a result of lockdown and limited medical access?
This would be an interesting intellectual exercise were it not for the original question that did not seem to be adequately asked and answered:
but what would be the consequences of switching off that important early warning system?
The answer to that may just be echoing the embryonic observations of doctors such as Ryan Cole.
The Mechanism
A clinical clue, albeit reported in low numbers at the moment, possibly supporting the work of Dominguez-Andres et al, and may be immunologically linked to Dr Cole’s observations, appeared as reactivation of Varicella Zoster Virus after vaccination for Sars-Cov-2:
Seven immunocompetent patients aged > 50 years old presented with herpes zoster (HZ) (ER: shingles) infection in a median of 9 days (range 7–20) after vaccination against SARS-CoV-2.
The occurrence of HZ within the time window 1–21 days after vaccination defined for increased risk and the reported T cell-mediated immunity involvement suggest that COVID-19 vaccination is a probable cause of HZ.
The data were consistent with the vaccine causing changes to the immune system that made the recipient more vulnerable to developing a herpes zoster (HZ) infection.
Furer et al in Herpes zoster following BNT162b2 mRNA COVID-19 vaccination in patients with autoimmune inflammatory rheumatic diseases:
a case series published in the Journal of Rheumatology also reported:
Potential mechanisms that might explain the pathogenetic link between mRNA-COVID19 vaccination and HZ reactivation are related to stimulation of innate immunity through toll-like receptors (TLRs) 3,7 by mRNA-based vaccines.
TLR signalling has been implicated during reactivation of herpes viruses, a process essential for these viruses to maintain themselves in the host.
Defects in TLR expression in patients suffering from diseases caused directly by herpes virus infection highlight the importance of these signaling pathways during infection and eventual disease progression.
The vaccine stimulates induction of type I INFs and potent inflammatory cytokines, which instigate T and B immune responses but may negatively affect antigen expression potentially contributing to HZ reactivation.
Both aforementioned studies implicate parts of the immune system post SARS-CoV-2 vaccination in HZ infection.
One might say: well, those studies have a significant number of older patients; the first study had a mean age of 77 yrs, and they have other health problems, and there may be other explanations.
For example, Methotrexate, a widely prescribed drug for immune mediated inflammatory disease that may be associated with older age has been questioned in the past for its effect on HZ infection, with some studies supporting a causal role, and others not.
... We must also note that HZ infection has also been observed in Covid-19 cases, and not just the elderly:
While there have been cases of varicella-zoster virus reactivation due to COVID-19 or COVID-19 vaccine inoculation in older individuals with pre-existing conditions,
this case report describes the first case of varicella-zoster virus reactivation on a healthy, young male in the absence of pre-existing conditions.
The mechanisms underlying varicella-zoster virus reactivation in patients with COVID-19 are unknown and should be further characterized.
Therefore, both Covid-19 infection and SARS-CoV-2 vaccination have been associated with HZ infection.
How many others have had a similar reaction but have gone unidentified?
Indeed, the mechanism needs to be characterised, and does it involve dysfunctional toll-like receptors? The above studies think so and blame the stimulation of specific toll-like receptors.
Toll-like receptors do play an important role in herpes infection; and TLR2, 3 & 9 specifically in Varicella Zoster infection; and any potential change in their function may therefore impact the body’s ability to control HZ infection.
... We can see from the above research that scientists are concerned that parts of the immune system are being negatively affected both by Covid-19 infection and SARS-CoV-2 vaccination, that may be leading to reactivation of Varicella infection.
Stimulation of toll-like receptors has been suggested, but the implicit design of the mRNA SARS-CoV-2 vaccines is such that they will stimulate certain toll-like receptors LESS; TLR 7 & 8 are RNA sensors and would be affected by Uridine changes to vaccine mRNA. TL4 would not.
Regardless, researchers have demonstrated that the response of innate immune cells to TLR4 and TLR7/8 ligands was lower after BNT162b2 (Pfizer) vaccination.
And that’s not good for the innate immune response.
Immune Dysregulation
The immune system is highly regulated with interconnected paths that immunologists are still discovering, and by changing one part you affect another.
If SARS-CoV-2 vaccination is changing something in our immune system, be it via changes in vaccine mRNA code and negatively affecting toll-like receptors or by other means, what else does it change in our immunity?
... SARS-CoV-2 vaccines ... switches off TLR 7 & 8 signaling, which the immune system needs to fight infection and cancer."
