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."

Association between regional selenium status and reported outcome of COVID-19 cases in China

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7197590/

"Immediately prior to the aforementioned publication, 2 separate articles provided evidence of a relation between GPX1 and Mpro, the main protease of SARS-CoV-2.

Mpro promotes formation of the viral replication complex and hence is a target of great interest for therapeutic intervention. The 3D crystal structure of MPro was recently described, leading to the identification of potential antiviral compounds through structure-assisted drug design and virtual screening.

Beginning from a pool of >10,000 compounds, the organoselenium compound, ebselen, emerged as the strongest inhibitor of Mpro. Ebselen is widely considered a GPX1 mimetic, as it reduces ROS via a mechanism similar to that of GPX1, whereby the selenol group is oxidized and subsequently reduced by glutathione.

Correspondingly, the potential involvement of GPX1 in COVID-19 was also highlighted in a separate study investigating the SARS-CoV-2 human protein interactome.

For the SARS-CoV-2 protease Mpro, screening was conducted using wild-type and a catalytically inactive mutant version of Mpro (Nsp5 C145A) to circumvent promiscuous covalent binding to the catalytic cysteine sulfhydryl group.

Three interacting proteins of high confidence were identified, histone deacetylase 2 (HDAC2), tRNA (guanine-26-(N-2))-dimethyltransferase (TRMT1), and GPX1. Taken together, the parallel findings of Mpro inhibition by the GPX1-mimetic ebselen and a physical interaction between Mpro and GPX1 further allude to an important protective role for GPX1 against COVID-19."

https://investors.modernatx.com/news-releases/news-release-details/moderna-completes-submission-biologics-license-application-us

from Moderna:

"IMPORTANT SAFETY INFORMATION

Do not administer the Moderna COVID-19 Vaccine to individuals with a known history of severe allergic reaction (e.g., anaphylaxis) to any component of the Moderna COVID-19 Vaccine.

Appropriate medical treatment to manage immediate allergic reactions must be immediately available in the event an acute anaphylactic reaction occurs following administration of the Moderna COVID-19 Vaccine. Monitor Moderna COVID-19 Vaccine recipients for the occurrence of immediate adverse reactions according to the Centers for Disease Control and Prevention guidelines (https://www.cdc.gov/vaccines/covid-19/clinical-considerations/managing-anaphylaxis.html).

Reports of adverse events following use of the Moderna COVID-19 Vaccine under EUA suggest increased risks of myocarditis and pericarditis, particularly following the second dose. The decision to administer the Moderna COVID-19 Vaccine to an individual with a history of myocarditis or pericarditis should take into account the individual’s clinical circumstances.

Immunocompromised persons, including individuals receiving immunosuppressive therapy, may have a diminished response to the Moderna COVID-19 Vaccine.

The Moderna COVID-19 Vaccine may not protect all vaccine recipients.

Adverse reactions reported in a clinical trial following administration of the Moderna COVID-19 Vaccine include pain at the injection site, fatigue, headache, myalgia, arthralgia, chills, nausea/vomiting, axillary swelling/tenderness, fever, swelling at the injection site, and erythema at the injection site.

The following adverse reactions have been reported following administration of the Moderna COVID-19 Vaccine during mass vaccination outside of clinical trials:

Severe allergic reactions, including anaphylaxis
Myocarditis and pericarditis

Available data on Moderna COVID-19 Vaccine administered to pregnant women are insufficient to inform vaccine-associated risks in pregnancy. Data are not available to assess the effects of Moderna COVID-19 Vaccine on the breastfed infant or on milk production/excretion.

There are no data available on the interchangeability of the Moderna COVID-19 Vaccine with other COVID-19 vaccines to complete the vaccination series. Individuals who have received one dose of Moderna COVID-19 Vaccine should receive a second dose of Moderna COVID-19 Vaccine to complete the vaccination series.

Additional adverse reactions, some of which may be serious, may become apparent with more widespread use of the Moderna COVID-19 Vaccine.

Vaccination providers must complete and submit reports to VAERS online at https://vaers.hhs.gov/reportevent.html. For further assistance with reporting to VAERS, call 1-800-822-7967. The reports should include the words “Moderna COVID- 19 Vaccine EUA” in the description section of the report."

WHO Chief: "WHO does not recommend jabbing children. We don't need more lockdowns." (Censored by YouTube)

YouTube slams its own supreme authoritative source, the WHO, for medical misinformation.

The video has just emerged from Brazil, but it was recorded two weeks back, at the G20 summit in Rome.

Brazil’s Poder 360 reported:

In the dialogue, mediated by a translator, Bolsonaro casts doubts on social isolation measures, the obligation to have a vaccine passport and on the vaccination of children. He also criticized the judiciary, which, according to him, concentrated powers on governors and mayors and said he was accused of genocide for “politics”…

Prof. Norman Fenton: Systemic flaws in COVID-19 vaccine efficiency and safety statistics

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SARS–CoV–2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro

This paper is showing that the (S) protein is inhibiting the DNA damage repair mechanisms. There are genetic predispositions to certain types of cancers, and certain cancers are due to DNA repair mechanism problems.

This is basically saying that DNA repair inhibition from the (S) protein leads to AIDS-like syndrome. AIDS-like syndrome means that there is an opportunistic infection that happens, especially in cancers, due to the downregulation of the immune system.

Cancer Route:
SARS-CoV-2 (S) protein ends up getting into the nucleus of your cells (the nucleus has pores called nucleopores). This is happening in high infection cases when human LINE-1 is expressed and this creates a higher chance of integration. Once integrated, the (S) protein inhibits the repair mechanism in the nucleus when DNA gets damaged. So, you'll have breaks in the DNA or misread/misdirected DNA code put in, and as it divides it starts to drift and this is where cancers arise.

So, if you don't have repair mechanisms in place, one line of problems is cancers, another issue is genetic disorders because when the cells are dividing it cannot repair them during the division process.

There is Gain-of-Function (GoF) and Loss-of-Function (LoF; the inability of something to work). A lot of genetic disorders/cancers happen due to LoF. LoF can happen due to a single nucleotide polymorphism (SNP) and loss of heterozygosity (LOH).

See: Gene Knockout & two-hit hypothesis

SNP/MNP changes the actual code and causes disease. Normally these are tumor suppressor genes, like P53, Wnt pathway, and BRCA1, for example, but if you don't have a repair mechanism working, when these cells are multiplying they will make mistakes and will have a loss of heterozygosity, resulting in the creation of cancers. see this paper: S2 Subunit of SARS-nCoV-2 Interacts with Tumor Suppressor Protein p53 and BRCA: an In Silico Study

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AIDS-like Syndrome Route:
The repair mechanism is very important in T and B-cells.

Antibodies created by T and B-cells are created by different types of code and recombined. To make this, there is something called the heavy chain; the heavy chain becomes the D-J segment, which turns into something smaller that then turns into the V-D-J segment. That turns into the actual code that will eventually make the protein. This turns into the transcription segment and it will then translate into becoming a protein and assemble.

Light chain and heavy chain. Two pieces to the heavy chain, two pieces to the light chain. Variable piece and the constant piece.

The light piece is made of L-V-J-C on your germline DNA. There are spaces between, it goes through a process and is rearranged and joined where that space is cut out. So it’s just L-VJ-C that is recombining inside of your cell. When it’s cutting/pasting, this is part of the repair mechanism. This turns into RNA. Then what happens is L-VJ-C-AAAA goes through a splicing where the space between the J and the C is taken out and it still has the poly(A). So, it will look like L-VJC-AAAAA with a poly(A) tail.

B-cells have isotype switching. B-cells can have a certain type of antibody and then switch to a new type of antibody. This switching happens through a signal, and that signal then, in its nucleus, begins to do the aforementioned recombination mechanisms. If it cannot do all of the recombination because the DNA repair is not working, then the switching mechanism doesn’t happen, so you have lower concentrations of all of the antibodies. Up front, if certain cells are infected and are unable to create the antibody because it’s not recombining, and the ones that are already there cannot switch due to SARS-CoV-2, then you cannot go from IgM to IgA or IgG, for example, so the switching slows down and over time you start to lose your antibodies.

In short, disruption of DNA repair mechanisms leads to opportunistic infections, cancers, AIDS-like syndrome.