If any of you can reach journalist Chris Snowden, do let him know I’d be more than happy to debate with him anywhere, anytime.
I can’t quite work out if he’s stupid or a criminal.
But anyone who writes “no one wanted a pandemic or lockdowns” is one or both of those things.
Cheers,
Mike
Ps: I can guarantee that, even if he learns of this challenge, he will decline it. His debate with Toby Young helped catalyse understanding of WHY lockdowns do not work.

https://capx.co/the-latest-smiley-myth-its-not-the-jabs-its-just-seasonality/

Bottom line: you can have SARSCoV2 and be healthy. The difference between healthy or Covid19 is in your innate immune system not in the virus. Spike protein plays a key role in this. Am I understanding this correctly?

Article16 June 2021

Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19

Sebastian J Theobald […] Jan Rybniker

Abstract

Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1β (IL-1β) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1β secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling."

https://www.embopress.org/doi/full/10.15252/emmm.202114150?s=09

See paper above for interaction between macrophages and spike protein. More on macrophages:

"Adenovirus (most common cause of pink eye) can remain latent in a host macrophage, with continued viral shedding 6–18 months after initial infection.

HIV infection

Macrophages also play a role in human immunodeficiency virus (HIV) infection. Like T cells, macrophages can be infected with HIV, and even become a reservoir of ongoing virus replication throughout the body. HIV can enter the macrophage through binding of gp120 to CD4 and second membrane receptor, CCR5 (a chemokine receptor). Both circulating monocytes and macrophages serve as a reservoir for the virus.[65] Macrophages are better able to resist infection by HIV-1 than CD4+ T cells, although susceptibility to HIV infection differs among macrophage subtypes.[66]"

Macrophage - Wikipedia
https://en.m.wikipedia.org/wiki/Macrophage

The 💉 🧲 may be due to graphene oxide in nanoparticles:

"Biocompatible N-acetyl cysteine [NAC] reduces graphene oxide and persists at the surface as a green radical scavenger"

https://pubmed.ncbi.nlm.nih.gov/30892320/

Managed to interview High Pim BBC. He didn’t have much to say. 😂

Find your courage at a time of fear.

#LOVEnotfear
Artwork by Suzy Magni
https://lovenotfearmankind.org
https://instagram.com/lovenotfearmankind
t.me/lovenotfearmankind

THIS GUY.......🤣🤣🤣

THE BIG WEEK DAY EVENT IS COMING TO LONDON!

We invite you to help make this the biggest ever weekday protest in our movement.
On the 19th of July @ 12pm we will be making a united stand as Boris delivers his 2nd speech to lift restrictions.

We stand in solidarity with all those that have suffered at the hands of the tyrannical government. We will be the voices for the voiceless. This ends when we say no!


#EndAllRestrictions
#NoMoreLockdowns
#WeStandUnited
#DividedWeFall
#DoNotComply

2001: "The illness known as Gulf war syndrome looks likely to have been caused by an illegal vaccine "booster" given by the Ministry of Defence to protect soldiers against biological weapons, according to the results of a new series of tests.
Scientists in the United States found that symptoms of the illness were the same for service personnel who received the injections whether or not they served in the Gulf."

https://theguardian.com/environment/2001/jul/30/internationalnews

Eine große Ehre, den Mann interviewen zu dürfen, der nicht nur Eric Clapton half, seine Erfahrungen mit der gefährlichen Corona-Impfung zu publizieren, sondern der auch Dr. Mike Yeadon Raum gibt, sich auf seinem Kanal frei zu äußern.

https://alschner-klartext.de/?p=5409

The Science has spoken:

1. Covid19 severity is about your pre-existing immune system, not about "catching" SARSCoV2

2. Many are already immune to severe Covid19 simply from having fought off the flu or CMV

"The COVID-19 pandemic has revealed a range of disease phenotypes in infected patients with asymptomatic, mild, or severe clinical outcomes, but the mechanisms that determine such variable outcomes remain unresolved.

In this study, we identified immunodominant CD8 T-cell epitopes in the spike antigen using a novel TCR-binding algorithm [TCR=T-Cell Receptor]. The predicted epitopes induced robust T-cell activation in unexposed donors demonstrating pre-existing CD4 and CD8 T-cell immunity to SARS-CoV-2 antigen. The T-cell reactivity to the predicted epitopes was higher than the Spike-S1 and S2 peptide pools in the unexposed donors.

[therefore the entire thinking behind spike protein gene therapy is flawed if not irrelevant]

A key finding of our study is that pre-existing T-cell immunity to SARS-CoV-2 is contributed by TCRs that recognize common viral antigens such as Influenza and CMV, even though the viral epitopes lack sequence identity to the SARS-CoV-2 epitopes.

This finding is in contrast to multiple published studies in which pre-existing T-cell immunity is suggested to arise from shared epitopes between SARS-CoV-2 and other common cold-causing coronaviruses. However, our findings suggest that SARS-CoV-2 reactive T-cells are likely to be present in many individuals because of prior exposure to flu and CMV viruses.

In conclusion, our study demonstrates strong pre-existing CD8 T-cell immunity in many unexposed donors contributed by the engagement of cross-reactive TCRs against common CMV [Cytomegalovirus] and flu antigens. The presence of high-quality cross-reactive TCRs can protect individuals by mounting an early CD8 T-cell response and clearing the virus.

"Vaccine" trials tested entirely the wrong thing: antibodies instead of T-cells.

"Many studies have indicated that short and long-term protection against respiratory viruses requires CD8 T-cell immunity and antibody response alone is not sufficient.. Our findings along with a recent report from Peng et al. showed that a higher CD8 T-cell response correlated with a mild disease compared to patients with severe disease.. On the contrary, high levels of neutralizing antibodies were associated with severe disease and ICU visits in many COVID-19 patients suggesting an imbalanced CD4 T-cell response is not optimal for protection"

https://www.nature.com/articles/s41598-021-92521-4

PHE: 25th June 2021

Covid19 deaths:

"Vaccinated": 70
Unvaccinated: 44

Draw your own conclusions.

https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/996740/Variants_of_Concern_VOC_Technical_Briefing_17.pdf

You are much more likely to test Covid19 positive if you are un-"vaccinated", however you are much more likely to die from Covid19 if you have been "vaccinated" compared to un-"vaccinated".

There is a name for this: vaccine enhanced disease or VED. Some call it pathogenic priming. Antibody-dependent enhancement is one of the mechanisms of how it happens. Non neutralizing antibodies effectively act as a Trojan horse for the virus. Remember: innate immunity is from T-cells not antibodies.

"The virus attaches itself to the human epithelial cells through noncovalent bonding of its spike protein with the angiotensin-converting enzyme-2 (ACE2) receptor on the host cell. We hypothesized that perturbing the functionally active conformation of spike protein through reduction of its solvent accessible disulfide bond, thereby disintegrating its structural architecture, may be a feasible strategy to prevent infection. Proteomics data showed that N-acetyl cysteine (NAC), an antioxidant and mucolytic agent been widely in use in clinical medicine, forms covalent conjugates with solvent accessible cysteine residues of spike protein that were disulfide bonded in the native state. In silico analysis indicated that this covalent conjugation perturbed the stereo specific orientations of the interacting key residues of spike protein that resulted in threefold weakening in the binding affinity of spike protein with ACE2 receptor. Antiviral assay using VeroE6 cells showed that NAC caused 54.3% inhibition in SARS-CoV-2 replication. Interestingly, almost all SARS-Cov-2 variants conserved cystine residues in the spike protein."

https://chemrxiv.org/engage/chemrxiv/article-details/60c753ec4c89190f3bad43ca

All warfare is based on deception.

The supreme art of war is to subdue the enemy without fighting.

Hence to fight and conquer in all your battles is not supreme excellence; supreme excellence consists in breaking the enemy's resistance without fighting.

-Sun Tsu