The AGILE Clinical Trial Platform

The AGILE clinical trial platform is a new type of study designed for pandemic drug testing which represents a world-first for infectious diseases – capable of testing multiple potential treatments in parallel and speeding up testing by pooling control data across patient groups.

[source]

https://stevekirsch.substack.com/p/according-to-dr-paul-offit-we-should

According to multiple independent analyses summarized here, the death rate from the COVID vaccines used in the US is at least 400 deaths per million doses. That’s 800 deaths per million fully vaccinated.

That makes the COVID vaccines the new leader by a long shot: the most dangerous vaccine ever created in history. They are 800X more dangerous than the smallpox vaccine with respect to death, and over 25X worse with respect to permanent disability (since the permanent disability rates are 10% higher than the death rate as you can see from the OpenVAERS redbox summary for US reports).

Dr. Chris Martenson: Mandates Have Nothing To Do With Public Health

Once again publicly available data demonstrate that vaccines are not reducing infectivity or transmission, two of the main criteria for an injection to be considered a vaccine. Public health officials are brazenly proclaiming these embarrassing facts, while at the same time continuing to parrot the mantra to get vaccinated and stop the spread.

At this point, anyone with a working brain can see that whatever the vaccine mandate push is for, that it is not about public health and stopping the transmission of COVID.

00:00 - Intro
00:58 - The Headlines
03:43 - The Study
04:51 - Vaccines Not All That Effective or Durable Against Delta
12:02 - Findings: Effective for only a while
19:04 - Permanent Vaccine Schedule May Thwart Natural Immunity
21:50 - VE & Symptomatic Covid…below zero?
24:04 - What a Proper Study Would Look Like
27:13 - My Personal “Terrain” Supplements
29:05 - Conclusions

[source]

Clade X Pandemic Exercise 2018 (Based on the Nipah Virus): A New Pandemic in the Making

https://www.euronews.com/next/2021/10/15/nipah-virus-could-cause-another-deadly-pandemic-warns-the-inventor-of-astrazeneca-s-covid-

note: see comment section for additional resources

https://cepi.net/news_cepi/nipah-virus-the-deadly-illness-without-a-vaccine/

"Given the urgent need for vaccines, Nipah virus became one of the first pathogens on CEPI’s target list following the coalition’s launch in 2017.

Since then, CEPI has invested up to US $100 million in four promising Nipah vaccine candidates, being developed by teams across academia and industry, including Auro Vaccines and PATH, Public Health Vaccines, the University of Tokyo, and the University of Oxford. Looking ahead, our overarching goal, as part of our $3.5bn forward-looking plan to reduce or even eliminate future epidemics and pandemics, is to develop a licensed Nipah vaccine or additional medical countermeasure.

Efforts to work towards this goal are already progressing. The CEPI-supported candidate, developed by Auro Vaccines & PATH, became the first to reach in-human trials in March last year. Conducted at the Cincinnati Children’s Hospital Medical Center in Cincinnati, USA, the study is a randomised, placebo-controlled, dose-finding study to investigate the safety, tolerability, and immunogenicity of their ‘HeV-sG-V’ Nipah vaccine candidate.

This vaccine contains a portion of a protein of Hendra virus, a henipavirus closely related to Nipah, and has been shown in preclinical studies to protect against both viruses. CEPI first announced up to $25 million of funding for this programme in May, 2018."

note: see comment section for additional resources. <<----------------

IncellDX Long COVID 19 (PASC) Research Video with Dr Bruce Patterson | Covid 19 Long Haulers

IncellDX research on long COVID 19 (PASC) has identified persistent S1 spike proteins from SARS-CoV-2 proteins in an immune cell called monocytes.

As the monocytes with COVID-19 proteins migrate and irritate these blood vessels, they release pro-inflammatory cytokines and chemokines to signal more inflammation. One of these chemokines is called CCL5 or RANTES and is secreted by both the immune and endothelial cells. Another is called FRACTALKINE, which acts like velcro, causing the monocytes to stick to endothelial cells.

They use an armamentarium of medications that targets specific cytokines that are unique to your immune profile, and they can now measure your response to these medications by using their patented long hauler index to guide your clinical management.

references: [01], [02], [03]

[source]

Dr. Paul Cottrell: Moderna using AI for vaccine development

additional resources:
[01], [02], [03], [04], [05], [06], [07], [08], [09]

BNT162b2 Vaccine: Possible Codons Misreading, Errors in Protein Synthesis and Alternative Splicing's Anomalies

https://www.bibsonomy.org/bibtex/25644c3d7200bd067966c310564c5808c/kill4thethrill?lang=de

This points to potential long-term risk in human health as it relates to the Pfizer-BioNTech mRNA COVID-19 gene therapy 'vaccine'. It’s possible that an excessive alteration aimed at an extreme increase in protein expression may be the source of errors in the assembly of the mRNA gene sequence.

Altering tRNA availability can lead to neurodegenerative diseases and upregulation of specific tRNAs drives metastasis by enhancing stability of transcripts enriched in their cognate codons.

Mistranslation has very serious consequences on the pathophysiology of a variety of diseases, including multiple sclerosis, neurodegeneration, mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes, Parkinson's disease, and cancer (genesis, growth acceleration and metastasis).

Mike Adams and Dr. Paul Cottrell Discuss Hoskins Effect & Boosters

Original antigenic sin (OAS), also known as antigenic imprinting or the Hoskins effect, refers to the propensity of the body's immune system to preferentially utilize immunological memory based on a previous infection or vaccination when a second, slightly different version of that foreign pathogen is encountered. This leaves the immune system "trapped" by the first response it has made to each antigen, and unable to mount potentially more effective responses during subsequent infections. Antibodies or T-cells induced during infections or vaccinations with the first variant of the pathogen are subject to a form of OAS, termed repertoire freeze.

The phenomenon of original antigenic sin (OAS) has been described in relation to SARS-CoV-2 and COVID-19 inoculations and has the potential to lead to Antibody Dependent Enhancement (ADE). In this scenario, the antibodies that the vaccine generated actually help the virus infect greater numbers of cells than it would have on its own. In this situation, the antibodies bind to the virus and help it more easily get into cells than it would on its own. The result is often more severe illness than if the person had been unvaccinated.

Because of the continued antigenic evolution of viruses, they accumulate mutations in the antibody epitopes and proteins that allow them to escape from immunity generated by prior vaccination or infection, a process known as “antigenic drift.” Antigenic drift occurs in unpredictable stops and starts, and at different rates for different types and subtypes of the virus.

The mechanisms that might be responsible for a negative effect of prior vaccination on vaccine effectiveness are not fully understood, but the finding that the magnitude of the negative effect depends on antigenic distance could be consistent with antigenic focusing. In this case, when sequentially exposed to (2) antigenically related viruses, the immune system focuses on the shared epitopes at the expense of novel epitopes on the second virus that might be important for the protection against a third, antigenically drifted virus. In contrast, a person who has not been previously vaccinated might mount a broader response against all of the epitopes in the vaccine.

Other potential mechanisms could include interference by prior immunity on antigenic presentation, or the “infection-block hypothesis.” In this case, prior vaccination reduces prior infections with the virus, which in turn would have provided more effective protection against subsequent drifted infection than the vaccine does, resulting in lower rates of illness in subjects with infection-based immunity than in those with vaccine-induced immunity.

Recent in silico research has shown that Carbon 60 (C60) fullerene displays inhibitory activity against various protein targets of SARS-CoV-2.

C60 interacts in the catalytic binding pocket of SARS-CoV-2 proteolytic enzyme 3-chymotrypsin-like protease (3CLpro), the main protease that is essential for the replication of SARS-CoV-2, which performs an important function to prime spike protein-mediated binding to human ACE2 and entry of the virus. Additionally, with SARS-CoV-2 RNA-dependent RNA polymerase (RdRp), C60 blocks the RNA synthesis pore and also prevents binding with Nsp8 co-factor (without this complex formation, RdRp cannot perform its initial functions). So, by blocking the RNA synthesis channel, the RNA synthesis procedure will be impossible.

Pfizer’s new antiviral, PF-07321332, and Ivermectin both block the activity of the SARS-CoV-2 3CLpro, but Ivermectin has additional mechanisms of action that inhibit key proteins of SARS-CoV-2 pathogenesis; these include blocking the recognition by the SARS-CoV-2 Receptor Binding Domain (RBD) of the Angiotensin-Converting Enzyme 2 (ACE2), the interactions with the two viral proteases 3CLpro and PLpro, and the SARS Unique Domain (SUD) non-structural protein.

C60 "buckyball" is characterized as a "free radical sponge" with an antioxidant efficacy several hundred-fold higher than conventional antioxidants. C60 helps the body replace four critical antioxidants that decrease through the process of aging (glutathione, catalase, CoQ10, and superoxide dismutase) and helps reduce ROS (Reactive Oxygen Species).

The immune system responds to viral infection by producing free radicals in the vicinity of viral particles in order to destroy them. However, this response can destroy both the pathogen and nearby healthy cells. Antioxidants can mute this response by reducing damage without impairing destruction of the pathogen. Antioxidants have been shown to enhance immune response, and this improved response reduces pathogenic viruses and can reduce the likelihood and severity of infection.

Antioxidants prevent or slow the damage to the cells caused by free radical reactions. The neutralization activity of radical molecules by antioxidants is achieved through their scavenging power by stopping chain reactions, peroxide decomposition, metal-chelating and induction of antioxidant enzymes.

Considerable interest has risen in the idea that oxidative stress (Os) is instrumental in the etiology of numerous human diseases. Os can arise through the increased production of reactive oxygen species (ROS) and/or because of a deficiency of antioxidant defenses and this may further worsen respiratory diseases (COVID-19 inclusive), especially when the level of free radicals is high.

Free radicals are a natural by-product of aerobic cell metabolism that the body can normally handle, but in the presence of a secondary condition, such as COVID-19, the abnormally excessive level of radicals may contribute in the progression and pathogenesis of the disease due to depletion of antioxidants.

A role for selenium-dependent GPX1 in SARS-CoV-2 virulence

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337667/

"Among the proteins most impacted by selenium status is glutathione peroxidase 1 (GPX1), a cytosolic selenoenzyme with known antiviral properties. Viral infection increases reactive oxygen species (ROS) production in host cells, which, if not counterbalanced by antioxidant defense mechanisms, leads to oxidative stress. Excess oxidative stress, in turn, augments mutation of the viral genome, which can lead to the emergence of more virulent strains.

GPX1 comprises a key defense against ROS, catalyzing the detoxification of hydrogen peroxide to water. In mice lacking the Gpx1 gene (Gpx1−/−), inoculation of a benign strain of coxsackievirus B3 (CVB3) led to viral genome mutations, increased virulence, and myocarditis, none of which were observed in wild-type mice.

Moreover, the Gpx1−/− model recapitulated the effect of a selenium-deficient diet in wild-type mice, promoting mutagenesis of the benign CVB3 strain into a virulent one. In addition, both selenium-deficient wild-type mice (6) and Gpx1−/− mice exhibit heightened inflammatory responses and more severe lung pathology in response to inoculation with influenza A, further indicating that GPX1 participates in molecular mechanisms protecting against viral infections of the respiratory tract. It is currently unknown whether SARS-CoV-2 is also modulated by GPX1 activity, but recent findings are highly suggestive."