 https://robynchuter.substack.com/ Molnupiravir causes transmissible mutations in SARS-CoV-2 Ok, so I told you masks don’t work to prevent respiratory virus infection and transmission, and now the latest Cochrane review has confirmed that they don’t work. Aaaaand, I told you that neither influenza vaccines nor COVID-19 vaccines prevent infection with, or transmission of, the viruses associated with them, and now Dr Anthony ‘I Am the Science’ Fauci himself has confirmed that neither they, nor any other vaccines for respiratory diseases caused by viruses that replicate predominantly in the respiratory mucosa, prevent infection or transmission. Let’s try for three for three. I told you back in May 2022 that Merck’s antiviral drug molnupiravir (sold under the brand name Lagevrio) generated mutated versions of SARS-CoV-2 that were shed in recipients’ nose and throat secretions, and could potentially lead to new, transmissible variants of unknown virulence. Our fearless drug regulator, the Therapeutic Goods Administration (TGA), airily dismissed the significance of this finding on the say-so of an unnamed ‘independent expert’: “The likelihood of mutations resulting in a more virulent strain of SARS-CoV-2 from treatment with molnupiravir over the long-term has not been assessed. It is less likely, but unproven, that virus mutation induced by molnupiravir will increase virulence of SARS-CoV-2.” Australian Public Assessment Report for Molnupiravir, p. 39 As a result of the TGA’s provisional approval of molnupiravir, over 380 000 prescriptions for this twenty year old drug which has never been used before due to concerns about its mutagenicity, had been issued in Australia by December 2022. Australian health authorities are still heavily pushing its use despite evidence of higher death rates in people treated with molnupiravir compared to placebo, and despite the National Clinical Evidence Taskforce in the UK recommending against it:  And now, an international team of researchers has produced compelling evidence that versions of SARS-CoV-2 with mutations consistent with the pattern induced by molnupiravir are showing up in global sequence databases, and that these viral variants are transmissible. To make sense of the new paper, which has not yet been peer reviewed but was considered significant enough to garner a write-up in Nature – one of the world’s most prestigious scientific journals – we need to do a quick review of molnupiravir’s mechanism of action. As explained in The great molnupiravir swindle, “It works by creating errors in the virus’s genetic code, known as mutagenesis. Each time the virus replicates in the presence of molnupiravir, more and more errors accumulate, eventually building up to an ‘error catastrophe’ that stops the virus from functioning.” The great molnupiravir swindle (The authors of the new paper dispute the notion of ‘error catastrophe’, and I’ve included their argument as a footnote for those interested in the finer points of this argument. 1 The mutations produced in the viral genetic code by molnupiravir are not random. Instead, they result in very specific substitutions in the four-letter nucleotide ‘alphabet’ that spells out the viral genetic code. Briefly, in RNA viruses including SARS-CoV-2, the genetic code is comprised of specific sequences of uracil (U), cytosine (C), adenine (A) and guanine (G). During the ‘reading’ of the genetic code that results in protein formation, A and U always pair with each other, while C and G pair with each other. Each three-nucleotide sequence (known as a ‘codon’) represents an amino acid, and the order in which the nucleotides appear dictates the order in which amino acids are strung together to form a protein. (There’s a good summary of this process here for those who want to delve deeper.) Molnupiravir results in substitution of adenine for guanine (a G-to-A mutation) and uracil for cytosine (a C-to-U mutation). This ‘mispelling’ of the viral code results in masses of mutant virions, most of which are non-viable – that is, they’re unable to do what viruses do to survive, which is to highjack the host cell’s protein-making apparatus in order to make more copies of themselves. However, some of these mutants are viable, and their signature mutations showed up in samples taken from participants in a clinical trial of molnupiravir. These same signature mutations can also be identified and tracked using the global viral sequencing databases GISAID and INSDC. And that’s exactly what the international team of researchers who wrote this recent paper did. They examined a mutation-annotated phylogenetic tree, which is a method for visually representing the relationships between the genetic sequences of various samples of SARS-CoV-2 that are uploaded to these global databases (see the example below), and identified branches with multiple G-to-A and C-to-U substitutions, consistent with molnupiravir-driven mutation.  Their analysis identified six key facts:
   In summary, mutations consistent with molnupiravir’s known mechanism of action, and of the same types that were found in the nasopharyngeal secretions of people who took the drug in a clinical trial, have shown up in global sequencing databases, since molnupiravir began to be prescribed, in the countries which are using it, in the age group for which it is approved, and in patterns which indicate that it is generating transmissible variants with high mutation rates.
When it comes to the implication of their findings, the study authors take a cautious approach. They point out that they have not proved that the use of molnupiravir is driving the mutations that they identified, nor that these mutations are intrinsically more dangerous or transmissible. They call for “public health authorities in countries showing these patterns [to] perform investigations to determine if these sequences or clusters can indeed be directly linked back to use of molnupiravir.” However, as coauthor Theo Sanderson, a computational biologist at the Francis Crick Institute in London, stressed, “I would say that our work closes down the possibility that these [molnupiravir-mutated] viruses can never be transmitted.” COVID drug drives viral mutations — and now some want to halt its use Rustem Ismagilov, a quantitative bioscientist at the California Institute of Technology in Pasadena who was not involved in the study, stressed that it “underscores the need to quickly measure any risk that molnupiravir poses in terms of sparking new variants, and to weigh them against the drug’s benefits”, adding “If we are playing Russian roulette, we’d better know our odds.” COVID drug drives viral mutations — and now some want to halt its use All I can say is, good luck with that one. I’d lay odds on hell freezing over before any study on the adverse effects of molnupiravir secures funding. Given molnupiravir’s lack of clinical benefit, the unanswered questions about its capacity to trigger cancer, and these latest findings that point to the strong possibility that it is driving variants with high mutation rates, any sane health authority would drop it like a hot brick. But the TGA continues to insist that it “meet[s] the high safety, efficacy and quality standards required for use in Australia.” One wonders how bad a drug has to be to not meet those standards. (Or perhaps the disqualifying criteria are actual safety and effectiveness, as with hydroxychloroquine and ivermectin.) Get the appWhat can we ordinary folk do in the face of the complete regulatory capture that is driving unsafe, ineffective and inadequately tested products into the mouths and arms of Australians?
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 Vaccine-induced antibodies don't confer immunity against viruses that replicate primarily in respiratory mucosa - like influenza and SARS-CoV-2. Says who? Says Anthony Fauci. In last week's post, I told you that masks don't work to prevent viral respiratory illness. Not for source control, not for infection protection, not when worn in a healthcare setting by properly-trained professionals. They Just Don't Work. Previously, I told you that influenza vaccines don't prevent infection with, or transmission of, influenza virus, here, and here. I also told you that COVID-19 'vaccines' don't prevent infection with, or transmission of, SARS-CoV-2 here, here, and here, and here, and I explained why here. In a nutshell, all the injected flu vaccines and all the COVID-19 'vaccines' currently on the market induce production of antibodies that travel in the blood (immunoglobulin G [IgG] and circulating immunoglobulin A [IgA]), but SARS-CoV-2 replicates in the mucous membranes that line our airways (the respiratory mucosa), not in the blood. The type of antibody that is required to stop this respiratory mucosal replication is secretory IgA (sIgA). None of the COVID-19 vaccines induce production of sIgA, and neither IgG nor circulating IgA can reach the respiratory mucosa. Here's the illustration of sIgA production and activity that I included in my previous article, Why COVID-19 “vaccines” will never end the pandemic which was published on 20 December 2021:  And now, a trio of crack scientists, including the recently-retired former head of the US National Institutes of Allergic and Infectious Disease, and Grand Chief Poohbah of Pandemia, Anthony S. Fauci, has published an article admitting that vaccines which only induce systemic antibodies (that is, antibodies travelling in the circulatory system) are next to useless against respiratory viruses that replicate in respiratory mucosa rather than causing systemic infection. Seriously. You can't make this stuff up. Here's what the mendacious midget who fully supported the sacking and social exclusion of anyone who declined the experimental COVID-19 transfection agents, and who has forcefully pushed for mandatory influenza vaccination in healthcare workers, had to say about how poorly these agents work, and why. First, flu vaccines don't really work: "Until the emergence of COVID-19, influenza had for many decades been the deadliest vaccine-preventable viral respiratory disease, one for which only less than suboptimal vaccines are available... Over the years, influenza vaccines have never been able to elicit durable protective immunity against seasonal influenza virus strains, even against non-drifted strains.4,5,6,7 Although current influenza vaccines reduce the risk of severe disease, hospitalization, and death to some degree [my note: they don't, as I explained in my previous article Flu vaccination and faith-based medicine, which also features a choice quote from the aforementioned Tom Jefferson on the 'rubbish' quality of flu vaccine clinical trials] their effectiveness against clinically apparent infection is decidedly suboptimal, ranging from 14% to 60% over the past 15 influenza seasons.1 Furthermore, the duration of vaccine-elicited immunity is measured only in months... As of 2022, after more than 60 years of experience with influenza vaccines, very little improvement in vaccine prevention of infection has been noted. As pointed out decades ago, and still true today, the rates of effectiveness of our best approved influenza vaccines would be inadequate for licensure for most other vaccine-preventable diseases.7" Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses Let that sink in. In many jurisdictions, certain occupations, including healthcare, aged care and disability care workers, are subject to mandatory flu vaccination. In Australia, some nursing homes won't let you visit your elderly relative if you don't produce proof that you've had a flu vaccine in the current flu season. But these jabs are so ineffective that they wouldn't pass licensure requirements if they weren't 'grandfathered' by decades-old approval processes. Next, COVID 'vaccines' don't really work, either: "As variant SARS-CoV-2 strains have emerged, deficiencies in these [COVID-19] vaccines reminiscent of influenza vaccines have become apparent. The vaccines for these two very different viruses have common characteristics: they elicit incomplete and short-lived protection against evolving virus variants that escape population immunity.12,13,14,15 Considering that vaccine development and licensure is a long and complex process requiring years of preclinical and clinical safety and efficacy data, the limitations of influenza and SARS-CoV-2 vaccines remind us that candidate vaccines for most other respiratory viruses have to date been insufficiently protective for consideration of licensure, including candidate vaccines against RSV, a major killer of infants and the elderly,16,17,18,19,20,21 parainfluenzaviruses, endemic coronaviruses,22 and many other ‘common cold’ viruses that cause significant morbidity and economic loss." Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses Is this the same Anthony Fauci who, in a panel discussion at the Milken Institute in 2019, appeared to be bemoaning the fact that the clinical trial process for flu vaccine development takes so long, and calling for a "disruptive" way of addressing this "problem"?  Watch Does anyone know what Teflon Tony actually believes??? (Side note: Construction of an mRNA vaccine manufacturing facility is already underway, on the grounds of Monash University in Melbourne. What do they plan to manufacture there? "COVID-19 booster shots as well as mRNA vaccines for other respiratory viruses such as influenza and respiratory syncytial virus (RSV)." Your taxpayer dollars, hard at work again. Another mRNA vaccine 'hub' is being created in Brisbane.) Update (19 February 2023):As reported by Alex Berenson, Moderna’s mRNA influenza ‘vaccine’ candidate has failed to demonstrate what is coyly called ‘non-inferiority’ to conventional flu vaccines, against influenza B strains, which account for the majority of flu cases in non-elderly adults. In addition, 70 per cent of trial participants who received the mRNA shot reported ‘solicited’ adverse reactions (i.e. adverse reactions that were explicitly asked about by trial staff) compared to 48 per cent of participants who received a conventional flu vaccine. The Moderna shot stimulated higher antibody production against influenza A strains than the conventional flu shot, but as discussed below, serum antibody levels are not an indicator of either immunity to influenza infection or protection against severe disease. Will this throw a spanner in the works of either the Melbourne or Brisbane mRNA manufacturing facilities? I doubt it. You can read Berenson’s report here:  https://alexberenson.substack.com/p/mrna-vaccines-fail-again?utm_source=substack&utm_campaign=post_embed&utm_medium=web Next, Fauci and his co-authors explain why vaccines against flu, COVID-19, RSV and other viruses associated with colds and flu are so wretchedly ineffective. The viruses involved in diseases like measles, mumps and chickenpox are transmitted by the respiratory route, but after an initial period of rapidly-accelerating replication in the respiratory tract (which roughly correlates to their incubation period), they make their way into the bloodstream and proceed to replicate there at a spectacular rate, resulting in significant viraemia (presence of infectious viral particles in the blood). These viral particles come in contact with many different cell types in multiple compartments of the immune system, resulting in a multifaceted immune response that usually confers life-long immunity. But cold and flu viruses are different: "In stark contrast, the non-systemic respiratory viruses such as influenza viruses, SARS-CoV-2, and RSV tend to have significantly shorter incubation periods (Table 1) and rapid courses of viral replication. They replicate predominantly in local mucosal tissue, without causing viremia, and do not significantly encounter the systemic immune system or the full force of adaptive immune responses, which take at least 5–7 days to mature, usually well after the peak of viral replication and onward transmission to others. SARS-CoV-2 'RNAemia' (circulation of viral RNA in the bloodstream, as is seen with most mucosal respiratory virus infections, as distinct from viremia, in which infectious viruses can be cultured from the blood), has been reported, and RT-PCR levels of viral RNA have been linked to severe disease,23,24 similar to studies of influenza RNAemia.25,26 As a result, the non-systemically replicating respiratory viruses, apparently including SARS-CoV-2,13,14,15 tend to repeatedly re-infect people over their lifetimes without ever eliciting complete and durable protection.27” Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses  In addition, both influenza and SARS-CoV-2 mutate too rapidly for any vaccine to effectively control their spread:
"Rapid antigenic drift affects the control of annual influenza epidemics8 and complicates the effort to produce broadly protective, ‘universal’ influenza vaccines. The SARS-CoV-2 spike protein has shown a similar plasticity, with the emergence of multiple variants with altered antigenicity33 that has complicated its control through current vaccination strategies.34" Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses Wait, it gets even better: "Taking all of these factors into account, it is not surprising that none of the predominantly mucosal respiratory viruses have ever been effectively controlled by vaccines." Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses Yes, the people who accused you of being a granny-murderer, supported mandates that took away your livelihood, and egged on your exclusion from society if you didn't accept the experimental transfection agent, are now saying, "Well, of course it doesn't really work, dummies! Smart scientists like us never thought it would!" Thank you for reading Empowered! This post is public so feel free to share it. Of course, the main thrust of the article is to call for the development of New! Improved! vaccines that - wait for it - mimic the body's own processes of developing mucosal immunity. Fauci and friend discuss the development of mucosal immunity, and the fact that none of the processes induced by vaccination are involved in it, at some length: "Many studies in humans and experimental animals, some before sIgA had been recognized,22,58,79,80,81 indicate that secretory mucosal immunity is generally more effective than systemic immunity in controlling mucosal respiratory viruses18,79,82 and that tissue-resident memory T cells can be effective in rapidly responding to mucosal infection.83 ... Nasal sIgA is the best correlate of protection in RSV challenge studies,18 even in the absence of systemic IgA-producing B cells. Similar results are seen with other viruses, including SARS-CoV-2.87,88,89,90 Although non-systemically replicating mucosal viruses elicit systemic effectors, including systemic IgA-producing plasma cells and in some cases high levels of serum IgA and IgG, neither circulating antibodies, plasmablasts, nor systemic B or T or T effector cells function optimally at mucosal sites. This is due in part to the dilution of transuded antibody and the fact that many such effector cells lack trafficking signals to these sites.85" Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses In other words, the natural response to respiratory viruses that infect mucous membranes is to pour out sIgA to stop the virus from replicating. The elements of the immune system that 'live' in the circulatory system, including B cells, T cells and blood-borne antibodies, don't make it through to the mucous membranes. Exactly as I explained in Why COVID-19 “vaccines” will never end the pandemic fourteen f#!*ing months ago. After some discussion of the inherent difficulty of developing a vaccine that induces both mucosal immunity (which is necessary for preventing infection with, and transmission of, respiratory viruses) and immunity within the lung (which is necessary for preventing serious illness), and an admission that flu vaccines are failures at both - "current influenza vaccines are suboptimal at both preventing infection and eliciting pulmonary immunity" - Fauci and Friends drop some good news for Big Pharma: "The implications for vaccinology are clear: preventing viral upper respiratory infection and limiting post-infection viral spread to contiguous respiratory compartments are both critical but may not be easily achieved with single vaccines." Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses If one vaccine won't do the trick, why not try two? What a bonanza for vaccine manufacturers! Will someone give Tiny Tony a seat on the board of PfizeRNAZeneca please? He's a marketing genius! Give a gift subscription But then comes the bombshell. After all of this hoo-hah about developing new you-beaut vaccines that simulate natural immunity, Fauci and Friends admit that they have no freakin' idea how to tell whether any such vaccines are effective or not because they don't fully understand how natural immunity against respiratory viruses works, and vaccine-induced 'immunity' simply doesn't work the same way: "Immune correlates of protection against mucosal respiratory viruses are incompletely understood, vary between viral strains and subtypes, with viral drift, and they exhibit inter-individual variation. In developing next-generation vaccines, we will need to identify strong immunologic correlates of protection against each mucosal respiratory virus and agree about their relevance to public health vaccination goals.80,101,102 Additional immune correlate studies in humans are clearly needed and should be a research priority. Following influenza infection in humans, studies have long identified serum and mucosal immunoglobulin correlates103,104,105 and T cell immune correlates.104,106,107 In contrast, a human influenza challenge study after vaccination with inactivated vaccines or live-attenuated influenza vaccine (LAIV), followed by LAIV challenge, was unable to find any immunologic correlates of protection.108" Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses So yeah, those flu vaccines they've been pumping into everyone for decades… well, nobody really knows what the heck they're doing. But send more money for research. They promise to use it wisely rather than - I don't know - funnel it to a lab controlled by the Chinese military to soup up bat viruses so they can infect humans. Honestly. In even more good news for vaccine manufacturers, the "next-generation vaccines" of Fauci's fever dream "may need optimized formulations, higher vaccine doses, greater frequency of vaccine administration, and overcoming immune tolerance challenges." More vaccines, more often, at higher doses, with more adjuvants. Yay for Big Pharma! If you have read up to this point and managed not to either vomit or become apoplectic with rage, congratulations. But what I'm about to tell you might just tip you over the edge. We already know how to raise secretory IgA productionThat's right, you don't need a fancy-schmancy vaccine to bump up your sIgA. You just need to make sure that:
 I hate to say 'I told you so' but I #$%^ING TOLD YOU SO! Back in the days when we still owned a television, my family and I used to enjoy watching The Big Bang Theory. This miniseries of important tidbits from current events in Clown World is named in honour of Sheldon Cooper’s immortal line from ‘The 21-Second Excitation’:  https://www.youtube.com/watch?v=vT-BO3y8szQ&embeds_euri=https%3A%2F%2Frobynchuter.substack.com%2F&feature=emb_logo
(Just as an aside, there’s a fascinating rabbit-hole you could go down regarding Zangen Pharmaceuticals, the drug company that The Big Bang Theory's Bernadette and Penny work for. For starters, there’s the name, which is shared with an Iron Cross-decorated Nazi general. And then there’s Bernadette’s disarmingly ingenuous revelations of Zangen’s involvement in mutating viruses to cross the species barrier, crossing Ebola with a common cold virus, and conducting unethical human experimentation. Is this merely dark humour, is it a confession, or is it predictive programming?) But enough about The Big Bang Theory. Let’s run through ‘This Week in I Told You So’. ‘I Informed You Thusly’#1: Masks Don’t WorkI told you that there is no reliable scientific evidence that face masks stop or even reduce the transmission of respiratory viruses, on multiple occasions. Ian Miller produced so many charts showing that neither cloth masks, nor N95s reduce case or death rates, no matter how high the compliance rates, that eventually he literally wrote the book on it. Paul Alexander compiled over 170 studies and articles demonstrating the ineffectiveness of masks for preventing respiratory virus transmission and illness, as well as the harms of masking. And now, the latest Cochrane Review on Physical interventions to interrupt or reduce the spread of respiratory viruses has confirmed what every previous Cochrane Review on the subject had found: masks don’t work when worn in the community. ‘In the community’ means outside of a healthcare setting – that is, people conducting their ordinary business, with no access to fit testing, and neither training in proper donning and doffing procedures nor the capacity to follow them. It’s also very likely that N95/P2 respirators don’t work, even when worn by properly-trained health care workers in settings that support correct use. (For those not familiar with Cochrane, it is the pre-eminent organisation for assessing the evidence base for medical and public health practice. Cochrane’s integrity and independence has been compromised in the last few years by its acceptance of donations from the Bill and Melinda Gates Foundation, which ultimately led to the expulsion of one of its prominent members, Peter Gøtzsche. Hence, Cochrane reviews are not as reliable as they used to be. It’s important to check the authorship of each review. The lead author of the mask review is Tom Jefferson, a stalwart defender of scientific integrity. Investigative journalists Maryanne Demasi and Paul Thacker have recently conducted interviews with Tom Jefferson, which are well worth reading as companion pieces to this post. Jefferson makes a particularly interesting revelation in the Demasi interview: the Cochrane organisation held up the publication of the previous update to this ongoing review, which was due to be published in early 2020, for seven months, in which time mask mandates had been imposed all over the world despite a total lack of evidence for their efficacy.) Here are the chief findings of the Cochrane review: 1. Masks don’t work to reduce symptoms of respiratory illness: “Wearing masks in the community probably makes little or no difference to the outcome of influenza‐like illness (ILI)/COVID‐19 like illness compared to not wearing masks (risk ratio (RR) 0.95, 95% confidence interval (CI) 0.84 to 1.09; 9 trials, 276,917 participants; moderate‐certainty evidence.” Physical interventions to interrupt or reduce the spread of respiratory viruses (Note that while the risk ratio of 0.95 suggests that mask wearing may reduce symptoms of respiratory illness by 5 per cent, the confidence interval includes 0, meaning that there is a good chance that there is is no difference between wearing and not wearing a mask.) 2. Masks don’t work to reduce lab-confirmed flu or COVID: “Wearing masks in the community probably makes little or no difference to the outcome of laboratory‐confirmed influenza/SARS‐CoV‐2 compared to not wearing masks (RR 1.01, 95% CI 0.72 to 1.42; 6 trials, 13,919 participants; moderate‐certainty evidence).” Physical interventions to interrupt or reduce the spread of respiratory viruses (Once again, the confidence interval includes zero.) 3. N95/P2 respirators don’t appear to work any better than cloth or surgical masks when it comes to preventing illness symptoms. There’s a slight signal of benefit, but the studies are too poorly-designed and reported to have confidence in them, and their results were all over the map: “We are very uncertain on the effects of N95/P2 respirators compared with medical/surgical masks on the outcome of clinical respiratory illness (RR 0.70, 95% CI 0.45 to 1.10; 3 trials, 7779 participants; very low‐certainty evidence). N95/P2 respirators compared with medical/surgical masks may be effective for ILI (RR 0.82, 95% CI 0.66 to 1.03; 5 trials, 8407 participants; low‐certainty evidence). Evidence is limited by imprecision and heterogeneity for these subjective outcomes.” Physical interventions to interrupt or reduce the spread of respiratory viruses 4. N95/P2 respirators don’t work any better than cloth masks when it comes to preventing influenza, whether in the general public or healthcare workers: “The use of a N95/P2 respirators compared to medical/surgical masks probably makes little or no difference for the objective and more precise outcome of laboratory‐confirmed influenza infection (RR 1.10, 95% CI 0.90 to 1.34; 5 trials, 8407 participants; moderate‐certainty evidence). Restricting pooling to healthcare workers made no difference to the overall findings.” Physical interventions to interrupt or reduce the spread of respiratory viruses In short, masks don’t work. And I told you so. Sneak preview of Part 2 of this miniseries: Teflon Tony Fauci admits that COVID and flu vaccines don’t work, and he knew along why they don’t. Stay tuned :). By: Robyn Chuter https://robynchuter.substack.com/p/i-informed-you-thusly-part-1  By: Robyn Chuter Health authorities have repeatedly stated that you're more at risk of developing myocarditis from COVID-19 than from the 'vaccine'. They lied. Remember when the COVID-19 ‘vaccines’ were sold to you as completely safe and effective? Sure you do.  https://www.youtube.com/watch?time_continue=1&v=-348hoZNidA&embeds_euri=https%3A%2F%2Frobynchuter.substack.com%2F&feature=emb_logo (Wow. That didn’t age well.) Remember when the authorities who told you they were completely safe and effective, admitted that they ‘very rarely’ cause myocarditis and pericarditis (collectively called ‘myopericarditis’)? You almost certainly do. Remember when those authorities told you that you should take them anyway, and give them to your kids, because the risk of developing myopericarditis (or other cardiac pathologies) as a complication of COVID-19 was greater than the risk of developing it as an adverse reaction to the experimental transfection agent? And remember when they told you that this very very rare myopericarditis was very very mild? I’ll bet you do. Remember when a cohort study of 23.1 million residents across four Nordic countries found that the risk of developing myocarditis in the 28 days after two injections of the Pfizer transfection agent was 5.31 times higher in males 16 to 24 years of age than it was in the pre-‘vaccination’ period, during which SARS-CoV-2 was widely circulating? In 16-24 year old males who received two shots of the Moderna product, the risk was 13.83 times higher than in the pre-‘vaccination’ period. Oh, you don’t remember this study being loudly trumpeted by the corporate media? Funny, that. It couldn’t possibly have anything to do with the fact that this study clearly showed that the risk of injection-induced myocarditis in young men far exceeded their risk of infection-induced myocarditis, could it? Remember when researchers found that the incidence of myopericarditis was 162.2 per million after dose two in US males aged 12–15 (that’s a risk of 1 case of myopericarditis per 6200 boys who received two doses), and 93 per million in males aged 16–17 (risk of 1 in 10,800), compared to a background rate of 2.1/million cases per week in boys); that 86.9 per cent of patients were hospitalised (does that sound ‘mild’ to you?); and that the risk of being hospitalised for myopericarditis after two shots of mRNA transfection agent was 2.8 times higher than the risk of being hospitalised for/with COVID in boys aged 12–15, and 1.6 times higher in boys aged 16–17? You mightn’t remember this one, because the pro-injection ‘experts’ tried to bury it, insisting that it was inappropriate to use the Vaccine Adverse Events Reporting System (VAERS), which was set up by the US government to detect safety signals from vaccines, to conduct research on a safety signal of a vaccine. Because Science™. Remember when Swedish researchers published a report on the autopsy findings on 37 people who had died at the Karolinska University Hospital of acute respiratory distress syndrome attributed to COVID-19, and found no replicating SARS-CoV-2 in the heart tissue of the deceased people, and no indications of myocarditis? “Furthermore, any sign of virus-induced cytopathic effects or any antiviral lymphocytic reaction typical for viral myocarditis was not detected in any cases. Also, signs of antiviral inflammation were not observed. Some studies claim there is a sign of lymphocyte infiltration in the Covid-19 heart [24]. For example, multifocal lymphocytic myocarditis was observed in a small fraction of the cases in a multicenter COVID-19 pathological study [25]. Furthermore, quantitative analysis of inflammatory infiltrates in COVID-19 hearts showed a higher number of CD68+ cells proposing that COVID-19 may cause a different type of myocarditis than conventional viral myocarditis, one that is associated with diffusely infiltrative monocyte/macrophage cells [26]. However, we didn’t detect any lymphocyte or granulocytic infiltration in the Covid-19 cohort as a hallmark of myocarditis.” Morphological changes without histological myocarditis in hearts of COVID-19 deceased patients No? You don’t remember that one? I guess it didn’t quite fit the narrative that COVID-19 myocarditis was much more dangerous than injection-induced myocarditis, did it? Remember when an international team of researchers published a review of all the reports that they could find of people who died of/with COVID-19 in the pre-injection era (a total of 548 deceased people), whose autopsy reports identified cardiovascular pathologies, and found a “low prevalence of myocarditis in COVID-19”? “The median reported prevalence of extensive myocarditis, multifocal active myocarditis, and focal active myocarditis were all 0.0%, and the median prevalence of inflammatory infiltrate without myocyte damage was 0.6%.” COVID-19–Associated cardiac pathology at the postmortem evaluation: a collaborative systematic review If you don’t remember it, that’s probably because it received next to no publicity. I wonder why. Finally, do you remember when Israeli researchers published a cohort study of almost 200 000 people, comparing rates of myopericarditis for which hospitalisation was required (i.e. moderate to severe cases), in the pre-injection era, in people who had had COVID-19 (defined as at least one positive PCR test for SARS-CoV-2; yes, I know this is a nonsensical diagnostic criterion but it’s the one the Branch Covidians use, so I’m happy to see them hoist with their own petard), to rates in those who had not… and finding that there was no increase in rates of either myocarditis or pericarditis in people who had had COVID? The rate of myocarditis in post-COVID-19 patients was 0.0046 per cent, while in the control group who had never had COVID-19 it was… 0.0046 per cent. 0.0056 per cent of post-COVID-19 patients were diagnosed with pericarditis, compared to 0.0088 per cent of controls. What? You haven’t heard of this study? Your doctor didn’t tell you about it, even though it was published in April of last year? Well, if you weren’t told about any of these studies before being injected with a novel RNA transfection agent, you weren’t given informed consent. If you were told that your teenage son’s risk of getting myocarditis was higher if he got COVID than if got the shot, neither of you was given informed consent (in fact, you were outright lied to). As the Australian Medical Professionals Society (AMPS) has pointed out in a letter sent to all Australian doctors on 11 January 2023, the federal government, the Australian Health Practitioner Regulation Agency and the Australian Immunisation Handbook all oblige Australian doctors and other vaccination providers to obtain informed consent before administering any treatment, including vaccines (or products deceptively labelled as vaccines). “For consent to be legally valid…It must be given voluntarily in the absence of undue pressure, coercion or manipulation…It can only be given after the potential risks and benefits of the relevant vaccine, the risks of not having it, and any alternative options have been explained to the person.” Australian Immunisation Handbook Furthermore, AMPS notified doctors that they do not have any government liability protection with respect to the novel COVID-19 transfection agents. And do you know what that means? If you, or a loved one, developed myopericarditis (or any other adverse event that your doctor should reasonably have known about) after receiving a COVID-19 injection, and you were not informed of the risk of this event prior to being injected, you can sue the person who administered the product to you. Can you imagine how quickly this entire disastrous enterprise could be stopped, if every single person who suffered an adverse reaction, and every single person who lost a loved one, sued the ‘vaccine’ provider for failing to give them informed consent? Professional indemnity insurance premiums would shoot through the roof, doctors and other vaccine providers would refuse to administer the shots for fear of being sued… and who knows, doctors might even remember that their role is to care for their individual patients, not to serve as the commissars of the biosecurity state. P.S. If you are part of, or know of, a legal firm willing to represent people injured by the experimental injections, please provide contact details in the comments section below. Legal firms who may be able to assist you with filing suit against a vaccine provider who did not give you informed consent: https://www.advocateme.com.au/ https://aflsolicitors.com.au/about http://woodburnsolicitors.com/home.html https://www.sydneycriminallawyers.com.au/  |
AuthorOur articles and rebuttal pieces are written by our writers on our volunteer team Archives
April 2023
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