It is an EXTREMELY important interview.
He knows. Everything.
Obviously he was right not to expose the lot in one go.
Even Tucker Carlson might not buy the truth.
I’m angling to see if he’ll interview me.

⬆️ TUCKER CARLSON: PLEASE INTERVIEW DR MIKE YEADON.

⬆️ 1+1=🚫💉

The CDC released a new guidance document "COVID-19 vaccine breakthrough case investigation. Information for public health, clinical, and reference laboratories".

Quote:
𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝘀𝗽𝗲𝗰𝗶𝗺𝗲𝗻𝘀 𝗳𝗼𝗿 𝘀𝗲𝗾𝘂𝗲𝗻𝗰𝗶𝗻𝗴 𝘀𝗵𝗼𝘂𝗹𝗱 𝗵𝗮𝘃𝗲 𝗮𝗻 𝗥𝗧-𝗣𝗖𝗥 𝗖𝘁 𝘃𝗮𝗹𝘂𝗲 ≤ 𝟮𝟴.

1st (false) Conclusion:
The False Positives-rate will fall dramatically ("yipee").

𝗧𝗵𝗲 𝗕𝗶𝘁𝘁𝗲𝗿 𝗣𝗶𝗹𝗹:
FP-rate will fall, yes - but only with the vaccinated, 2 datasets are created, cloaked and compared as the same, Jabs will appear to work.

𝗧𝗵𝗲 𝗨𝗹𝘁𝗿𝗮𝗯𝗶𝘁𝘁𝗲𝗿 𝗣𝗶𝗹𝗹:
Only those COVID-19 cases are reported when people have been vaccinated + hospitalised/dead.

Source:
https://www.cdc.gov/vaccines/covid-19/downloads/Information-for-laboratories-COVID-vaccine-breakthrough-case-investigation.pdf

⬆️ What this means is that there will be two types of test, one applied to the vaccinated (the correct parameter of cycle thresholds) and one to the non vaccinated (the wrong parameter leading to 90% false positives). Correct @bobby_network?

This is not good news for mRNA vaccines. Non-neutralizing antibodies are those which cause vaccine enhanced disease or ADE.

"In summary, we demonstrate that the antibody responses to SARS-CoV-2 mRNA vaccination comprise a large proportion of non-neutralizing antibodies and are co-dominated by NTD and RBD antibodies. The NTD portion of the spike represents, thus, an important vaccine target. Since all viral variants of concern are heavily mutated in this region, these observations warrant further attention to optimize SARS-CoV-2 vaccines. Finally, broadly cross-reactive mAbs to β-coronavirus spike proteins are induced after vaccination, and suggest a potential development path for a pan-β-coronavirus vaccine."

https://www.medrxiv.org/content/10.1101/2021.03.07.21253098v2.full

"For a given concentration of antibody and a specific targeting domain, the stoichiometry [reactants and products in chemical reactions] of antibody engagement on a virion is dependent on the strength of interaction between antibody and antigen [substance that when introduced into the body stimulates the production of an antibody]. ADE [antibody dependent enhancement or vaccine enhanced disease] is induced when the stoichiometry is below the threshold for neutralization. Therefore, higher affinity antibodies can reach that threshold at a lower concentration and mediate better protection.

We argue that ADE should be given full consideration in the safety evaluation of emerging candidate vaccines for SARS-CoV-2."

The potential danger of suboptimal antibody responses in COVID-19 | Nature Reviews Immunology
https://www.nature.com/articles/s41577-020-0321-6

a | In antibody-mediated viral neutralization, neutralizing antibodies binding to the receptor-binding domain (RBD) of the viral spike protein, as well as other domains, prevent virus from docking onto its entry receptor, ACE2. 

b | In antibody-dependent enhancement of infection [ADE], low quality, low quantity, non-neutralizing antibodies bind to virus particles through the Fab domains. Fc receptors (FcRs) expressed on monocytes or macrophages bind to Fc domains of antibodies and facilitate viral entry and infection. 

Monocytes and macrophages as the most important cells of the innate arm of the immune system play a substantial part in the body's defense against viral infections. They mainly respond to the microbial antigens by producing inflammatory mediators to remove pathogens and repair tissue injury.
https://pubmed.ncbi.nlm.nih.gov/33454368/

Monocytes and macrophages are very closely related cells with a few important distinctions and different use cases. Put simply, monocytes are macrophages in the blood; macrophages are monocytes in tissue.
https://cellero.com/blog/ask-scientistwhats-difference-human-monocytes-macrophages/

c | In antibody-mediated immune enhancement [AMIE], low quality, low quantity, non-neutralizing antibodies bind to virus particles. Upon engagement by the Fc domains on antibodies, activating FcRs with ITAMs initiate signalling to upregulate pro-inflammatory cytokines and downregulate anti-inflammatory cytokines. Immune complexes and viral RNA in the endosomes can signal through Toll-like receptor 3 (TLR3), TLR7 and/or TLR8 to activate host cells, resulting in immunopathology.

GEERT VANDEN BOSSCHE'S "LAST REPLY" TO MIKE YEADON

Geert Vanden Bossche (DVM, PhD)

"Second and last reply to M. Yeadon

Michael Yeadon’s rhetoric that mass vaccination campaigns do not have the potential to promote circulation of more infectious immune escape variants and that more infectious variants are not problematic are not based on sound immunological grounds at all. This will be my second but last reply to his erroneous and misleading interpretations. I hate to do this since this may leave the public with the opinion that people like me have nothing else to do than to focus on their own ego, although nothing is less true. However, when the most compelling arguments for my warning about the potentially disastrous consequences of mass vaccination are wiped from the table with scientifically hollow and invalid arguments, one has no choice but to react. Now, more than ever before, criticism is indispensable to build and consolidate a consensus on why mass vaccination campaigns (using the current vaccines in the heat of a pandemic caused by a highly mutable virus) are highly problematic. However, it doesn’t help when people bring to the table arguments that are scientifically incorrect.


Yeadon is basically not understanding the difference between viral escape from protection-blocking immunity and viral escape from infection-/ transmission-blocking immunity.

more infectious variants will make rise the infection rate in the population, thereby increasing the likelihood that previously asymptomatically infected people get re-infected by a variant within a few weeks (1-6w) after their primary infection. This is at risk of enhancing their susceptibility to the disease as their natural Abs may be sufficiently suppressed by their suboptimal S-specific Abs to no longer be able to eliminate the virus via innate immune cells (most likely NK cells). Yeadon may want to educate himself on natural/ innate Abs and their relevance in fighting a multitude of different pathogens, not just viruses and not only CoV but, for example, also Influenza virus.


The bottom-line is that Yeadon is far more eloquent than I am and that I would certainly prefer if he would lead the discussion when it comes to opposing the madness of mass vaccination campaigns. However, as long as he’s mistaken about the high likelihood for these campaigns to drive the adaptation of more infectious variants and the issue that comes with those, I cannot concur with his strategy for countering the mass vaccination program."

https://www.geertvandenbossche.org/post/second-and-last-reply-to-m-yeadon

EXPOSING THE LIE OF ASYMPTOMATIC TRANSMISSION, ONCE AND FOR ALL

Video features Dr. Mike Yeadon, Nick Hudson (PANDA- Pandemics, Data and Analysis), Reiner Fuellmich, Tony Fauci, Maria Van Kerkhove (WHO), Dr. Henry Ealy (IPAK), Prof. Emeritus of Immunology Beda Stadler, and Dr. Patrick Phillips MD

Here is the video in Bitchute:

https://www.bitchute.com/video/lIj22KttYq7z/
…………………………………………………………..................

Dr Mike Yeadon may not reply to GVB'S "last reply", so I will with my basic understanding, being a student of Mike myself. Something really stood out to me from GEERT VANDEN BOSSCHE's "last reply". It is this paragraph, especially the last part:

"Again, he doesn’t seem to capture that even a single mutation can make a big difference when it enables enhanced infectiousness and is comprised within a variant that is repeatedly exposed to conditions that precisely exert immune pressure on viral infectiousness. Again, in terms of clinical protection and recovery from disease, CTLs can deal with all of them and I never pretended the opposite. However, more infectious variants will make rise the infection rate in the population, thereby increasing the likelihood that previously asymptomatically infected people get re-infected by a variant within a few weeks (1-6w) after their primary infection. This is at risk of enhancing their susceptibility to the disease as their natural Abs may be sufficiently suppressed by their suboptimal S-specific Abs to no longer be able to eliminate the virus via innate immune cells (most likely NK cells) ."

What GVB's is referring to, in the last section, is suboptimal antibodies. This is precisely what I was writing about yesterday in explaining the two mechanisms of vaccine enhanced disease or VED
1 Non neutralizing antibody dependent enhancement leading to a more severe disease or ADE
2 Low quality, low quantity antibody mediated immune enhancement leading to cytokine storm or AMIE

The above, especially number 2, is how I understand the reason Jordan Peterson was given to send him off to get injected even if he already had Covid19. I do not think this was in his best interest nor scientifically correct

I think what GVB is referring to, without naming them, are precisely ADE & AMIE. Why does he not call them by their real name? I think he is referring to ADE & AMIE because GVB gives the indication of a 1-6 week window of reinfection. Let's think through this.

If the immune system produces antibodies in response to the virus, then the antibody counts are indeed highest in those 1-6 weeks post infection which GVB is mentioning. So he is acknowledging that if the antibodies in that period of time are sub-optimal, or non neutralizing they may enhance disease if there was a reinfection. GVB says the reinfection is by a variant, whereas I believe the variant is not the issue here, the issue is why is the cellular response, naive and killer T cells or NK (natural killer) cells not able to prevent a reinfection? I think the answer is precisely the sub-optimal or non neutralising antibodies overwhelming the cellular response through the mechanisms of ADE & AMIE.

But why would the antibodies be suboptimal? There are two reasons in my view apart from the single variant reason that GVB is offering us. These are:
1 The infection was asymptomatic or not severe enough or to create enough or good quality antibodies: antibodies are low quantity and perhaps even low quality as the immune system didn't need to produce them: it fought the virus off with T & NK cells.
2 They are suboptimal because they are induced by a vaccine which creates non neutralizing antibodies.