The Playground

Quote

The natural version is more robust No, it is not.

Jed, you're undoubtedly well read and competent scientist in field of cold fusion, but regarding vaccination you're still arguing like small kid when being taken away from his toy. Do you really believe that immune system trained to single spike protein from whole virus will work as precisely and reliably like immune system trained to all other 29 proteins at the same moment? The white immune cells trained to spike protein only would behave like white cops, who just learned from criminal statistics that blacks are bad because of their colour: such a cops will indeed attack many innocent blacks and vice versa, they will leave white criminals unpunished. Simply because they learned to spot and recognize criminals by single aspect of their existence.

Another problem of immunity trained to single protein (which m-RNA vaccines do) is, once this protein mutates, then whole the vaccination becomes toothless as we can already observe with delta etc variants of coronavirus.

The people like Jed can not indeed make too much damage on some burrowed forum - the actual problem for human population arises when healthcare system becomes controlled with similar ignorants at global scale.

Quote from Zephir_AWT

The people like Jed can not indeed make too much damage on some burrowed forum - the actual problem for human population arises when healthcare system becomes controlled with similar ignorants at global scale.

What is unluckily the case in almost all western countries. Sweden did a great job, Switzerland did less but still much more than most others. Free (of mask no 3G) skiing over Christmas new year!

To many Nazi doctors e.g. in Germany now block the media!

Quote from Wyttenbach

It (thapsigargin) is highly toxic and carcinogenic. Its used in lab test as a C2 inhibitor. (See Wiki)

Correctly said:: Vaccines do this. But not Pfizer, Oxford-Astra/J&J CoV-19 gene therapies that produce monoclonal antibodies only...And no usable immune memory cells... Moderna is a bit broader.

It's toxic to sheep, it's being used as a treatment for skin cancer and to target tumor formation. In Covid it would be given over 3-5 days at low concentrations. Just trying to show botanicals offer better protection than the latest and greatest vaccines!

Quote from Alan Smith

https://www.japantimes.co.jp/n…cx_1&cx_artPos=0#cxrecs_s

Why did Japan’s fifth and biggest wave of the coronavirus pandemic, driven by the supercontagious delta variant, suddenly come to an abrupt end following a seemingly relentless rise in new infections? And what made Japan different from other developed countries that are now seeing a fresh surge in new cases?

According to one group of researchers, the surprising answer may be that the delta variant took care of itself in an act of “self-extinction.”

Three months after the delta variant spurred record daily nationwide caseloads of nearly 26,000, new COVID-19 infections in Japan have plummeted, dropping below 200 in recent weeks. Highlighting that drop was the fact that no deaths were reported on Nov. 7 — the first time that had happened in about 15 months.

Many scholars point to a variety of possibilities, which include one of the highest vaccination rates among advanced countries with 75.7% of residents fully vaccinated as of Wednesday. Other potential factors are the social distancing and mask-wearing measures that are now deeply embedded in Japanese society.

But the chief reason may be related to the genetic changes that the coronavirus undergoes during reproduction, at a pace of around two mutations per month. According to a potentially revolutionary theory proposed by Ituro Inoue, a professor at the National Institute of Genetics, the delta variant in Japan accumulated too many mutations to the virus’s error-correcting, non-structural protein called nsp14. As a result, the virus struggled to repair the errors in time, ultimately leading to “self-destruction.”

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Low genetic diversity may be an Achilles heel of SARS-CoV-2

Low genetic diversity may be an Achilles heel of SARS-CoV-2

Scientists worldwide are racing to develop effective vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the…

www.pnas.org

Scientists worldwide are racing to develop effective vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID-19 pandemic. An important and perhaps underappreciated aspect of this endeavor is ensuring that the vaccines being developed confer immunity to all viral lineages in the global population. Toward this end, a seminal study published in PNAS (1) analyzes 27,977 SARS-CoV-2 sequences from 84 countries obtained throughout the course of the pandemic to track and characterize the evolution of the novel coronavirus since its origination. The principle conclusion reached by the authors of this work is that SARS-CoV-2 genetic diversity is remarkably low, almost entirely the product of genetic drift, and should not be expected to impede development of a broadly protective vaccine.

Although errors introduced during genome replication are a major source of genetic variation in all virus populations, limiting the fitness costs of accumulated errors is especially critical for coronaviruses, the RNA genomes of which are the largest known. For this reason, coronaviruses evolved nonstructural protein 14 (nsp14), which accompanies viral replicases during RNA synthesis and excises misincorporated ribonucleotides from nascent strands before they can be extended, thus preventing errors from becoming permanent. This error-correcting capacity was unknown among RNA viruses prior to its discovery in SARS-CoV-1 (2, 3), and it contributes to a replication error rate more than 10-fold lower than that of other RNA viruses (4, 5). This activity also likely contributes to the low genetic diversity of SARS-CoV-2, although to our knowledge nsp14 function in the novel coronavirus has yet to be investigated.

For many viruses, surface glycoproteins contain not only elements required for specific binding of cellular receptors, membrane fusion, and virus entry into the host cell but also epitopes recognized by neutralizing antibodies produced as part of an effective adaptive immune response. Hence, tracking genetic variation in the SARS-CoV-2 surface glycoprotein is of paramount importance for determining the likelihood of vaccine effectiveness or immune escape. To put this variation in perspective, Fig. 1 shows a graphical illustration of comparative genetic diversity among surface glycoproteins of select human pathogenic viruses, including SARS-CoV-2, correlated with the availability and effectiveness of respective preventive vaccines.

A Judge Stands up to a Hospital: "Step Aside" and Give a Dying Man Ivermectin

A Chicago-area judge saved a grandfather's life with the single question that exposes hospitals blocking doctors from using a safe, FDA-approved drug: Why?

rescue.substack.com

This story was posted here when the daughter was fighting (unsuccessfully) the hospital to allow her dying father be given IVM. Here is an update:

"The hospital ultimately stepped aside. Dr. Alan Bain, an internist, administered a five-day course of 24 milligrams of ivermectin, from November 8 through November 12."

"Ng, who with his wife, Ying, had come from Hong Kong to celebrate their granddaughter’s birthday, was able to breathe without a ventilator within five days—he, in fact, removed the endotracheal himself. He left the ICU Tuesday, November 16, and, although confused and weak, was breathing Sunday without supplemental oxygen on a regular hospital floor."

“Every day after ivermectin, there was accelerated and stable improvement,” said Dr. Bain, who administered the drug in two previous court cases after hospitals refused. “Three times we’ve shown something,” he told me. “There’s a signal of benefit for ventilator patients.”"

Quote from THHuxleynew

Even well-read commentators like W here confuse vaccine efficicacy against original COVID (outstanding) with vaccine efficacy against delta (much less good). I'll bet mots people, including be, do not remember always whether as particular set of data is related to delta, original, alpha, or some combo.

Huh? It was well known that vaccine efficacy was waning well before Delta arrived on the scene.

Even in the Lancet study that looked at recent household transmission in September, the virus was cleared faster with the Delta infection than pre-Alpha infection in the vaccinated. There was also moderate evidence that Delta infection growth was slowed more that pre-Alpha infection growth in the vaccinated.

DEFINE_ME

Maybe it's time to blame the vaccines for their waning efficacy against infection and transmission, rather than the variants.

Quote from Shane D.

“Three times we’ve shown something,” he told me. “There’s a signal of benefit for ventilator patients.”"

That is why the big pharma mafia invested at lot of money to discredit El-Gazzar that did show 98% survival effect for Ivermectin on ICU patients! "Only", 80% for HCQ. Of course the dose was 4x .. 6x. 2x is low.

Merck’s Molnupiravir Data Bombshell—Absolute Risk Reduction of 3%

Merck’s Molnupiravir Data Bombshell—Absolute Risk Reduction of 3%

A recent material update from Merck & Co based on its MOVe-OUT study of molnupiravir (MK-4482, EIDD-2801), the oral antiviral experimental medicine

trialsitenews.com

A recent material update from Merck & Co based on its MOVe-OUT study of molnupiravir (MK-4482, EIDD-2801), the oral antiviral experimental medicine originally developed by scientists at Emory University then licensed to Ridgeback Biotherapeutics—and then further licensed to Merck during the pandemic—reveals significantly less promise than previously reported. On Oct. 1, Merck announced an approximate 50% reduction in hospitalization and deaths based on aggregated data of 1,433 patients. On Oct. 12, TrialSite reported on Merck’s submission of application for emergency use authorization (EUA) to the U.S. Food and Drug Administration (FDA) based on the promising data the company disclosed back on Oct. 1. Merck shared that the MOVe-OUT study’s independent Data Monitoring Committee stopped the study as the planned interim data analysis of MOVe-OUT revealed molnupiravir reduced the risk of hospitalization or death by approximately 50%. They published that 7.3% of patients who received the drug were either hospitalized or died through Day 29 post-patient randomization (28/385) as compared to 14.1% of the placebo-treated patients (53/377). Fast forward to Friday, Nov. 26, and the company’s most recent data reveals the risk of hospitalization or death from 9.7% in the placebo group (68/699) to 6.8% (48/709) in the molnupiravir for an absolute risk reduction of 3.0%—that’s right; the true risk reduction this drug affords for billions of dollars stands at 3%.

Before and After

What a difference just over a month makes. TrialSite provides a before and after summary below.

Merck Report Merck Nov. 26 Report

Relative Reduction in Risk of Hospitalization or Death (relative) 50% (reported Oct 11) 30%

Placebo Vs. Molnupiravir 14.1% (53/377) placebo7.3% (28/385) molnupiravir 9.7% (68/699) placebo6.8% (48/709) molnupiravir

Deaths in placebo & study drug groups 0 who received molnupiravir8 who received placebo 1 death in molnupiravir group9 deaths in placebo group

Absolute Risk Reduction 3%

Note that Merck didn’t report absolute risk reductions in their Oct. 1 press release announcing the interim results or their Oct. 11 press release announcing their EUA. A telling figure surfaces in this latest Nov. 26 press release, the absolute risk reduction demonstrated in this study was 3% (95% CI; 0.1, 5.9; nominal p-value = 0.0218) versus the relative risk reduction of 30% (relative risk 0.70; 95% Cl; 0.49, 0.99).

Major Implications?

Frankly, the data backing this product went from good to mediocre at best, if not worse. Merck did submit this data right before the FDA published documentation on Friday meant for sharing with an outside expert panel who will come together Tuesday to discuss the recommendation of the drug’s authorization. Then, on Nov. 30, the FDA’s Antimicrobial Drugs Advisory Committee meets.

What will this group of experts discuss? The FDA shared, among other things, whether the risks of the investigational product outweigh any perceived benefits as well as discuss appropriate patient populations given any of the drug’s limitations—more on that below.

The Press Release

Merck’s recent press release was understandably short. Discounting the material decline in data, the company reminds all that the study was properly discontinued as “definitive evaluation of efficacy” was met during that planned interim analysis.

Nonetheless, the company’s quest for that massive COVID-19 antiviral market continues as it declared, “the interim analysis and the additional analyses support the efficacy and overall favorable risk-benefit assessment of molnupiravir for the treatment of mild-to-moderate COVID-19 in adults with high risk for disease progression.”

Wheeling and Dealing Regardless

All based on the initial interim data, Merck’s commercial business executives have crisscrossed the globe doing deal after deal. From Southeast Asia to Europe, the company has been selling billions worth of the experimental product, including a $1.2 billion commitment from the U.S. government. The company structured a multifaceted deal with generic producers to make the product in India. TrialSite even reported that COVID-19 patients in Vietnam’s Ho Chi Minh City were given the drug as part of a real-world care pilot (experiment?) with no traditional clinical trial underpinnings.

Competition

At one point, growing interest in ivermectin elicited a well-funded, orchestrated, and integrated public relations campaign to completely delegitimize the use, off-label via physician prescription, of that currently approved, repurposed prospect. A few key studies (COVID-OUT, ACTIV-6 and PRINCIPLE) include the widely used drug targeting parasitic infections; however according to TrialSite experts, all of the studies are severely underdosed, hence more than likely destined to fail.

How Much Money at Stake?

TrialSite has reported that Merck plans to produce 10 million courses by the end of 2021 and at least 20 million courses in 2022. Merck inked a deal with the U.S. at $700 per course, and millions of courses have already been purchased. TrialSite forecasts at least over $10 billion is at stake over the next couple years.

The company’s stock price declined 3.5% to $79.39 in early AM trading.

Just a reminder: How big pharma aka CDC/FDA just did wave through harming children with monoclonal RNA gene therapies.

14 ACIP Members Who Voted to Jab Your Young Children — and Their Big Ties to Big Pharma

On Nov. 2, members of the Centers for Disease Control and Prevention’s vaccine advisory committee voted 14–0 to recommend Pfizer’s pediatric COVID shot for…

childrenshealthdefense.org

Quote from Fm1

nominal p-value = 0.0218) versus the relative risk reduction of 30% (relative risk 0.70; 95% Cl; 0.49, 0.99).

Merck-vectin already failed in more than two hospital studies and in one Indian outpatient study. So they now present the "best" of 4 studies.

Eben black cumin gives you a 75% risk reduction at a fraction of the cost and 0 risk. Why should somebody take this crap???? that gives at best 30% risk reduction.

Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells

Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells - Nature Immunology

During homeostasis TH1 cells activate a cell-intrinsic inflammatory shutdown program and shift to IL-10 production. Chauss et al. find that this TH1…

www.nature.com

Abstract

The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

Discussion

We showed that cell-intrinsic complement orchestrates an autocrine/paracrine autoregulatory VitD loop to initiate TH1 shutdown. VitD causes genome-wide epigenetic remodeling, induces and recruits TFs, including STAT3, c-JUN and BACH2, which collectively repress TH1 and TH17 programs and induce IL-10 via IL-6–STAT3 signaling. This program is abnormal in lung helper T cells of patients with severe COVID-19, which show preferential TH1 skewing and could be potentially exploited therapeutically by using VitD as an adjunct treatment.

IFN-γ-producing airway helper T cells are key components of immunity to coronaviruses, including SARS-CoV1 and MERS-CoV20. TH1-polarized responses are also a feature of SARS-CoV2 in humans24 and severe COVID-19 is accompanied by prolonged, exacerbated, circulating TH1 responses21. Complement receptor signaling is a driver of TH1 differentiation and required for effective antiviral responses12,42. C3 cleavage generates C3b, which binds CD46 on T cells. We have previously shown that the lungs in COVID-19 are a complement-rich microenvironment, that local CD4+ T lymphocytes have a CD46-activated signature13 and show here that these T cells are TH1-polarized. Pro-inflammatory function is important for pathogen clearance, but a switch into IL-10 production is a natural component during successful transition into the TH1 shutdown program and reduces collateral damage16. Inability to produce IL-10 results in more efficient clearance of infections but severe tissue damage from uncontrolled TH1 responses results in death2. The benefits of remediating inflammatory pathways in severe COVID-19 is demonstrated by successful trials of dexamethasone, an immunosuppressive drug that reduces mortality1.

VitD has pleiotropic functions in the immune system, including antimicrobial as well as regulatory properties, which are cell- and context-dependent43,44. VitD deficiency is associated with higher prevalence and worse outcomes from infections, including influenza, tuberculosis and viral upper respiratory tract illnesses17, as well as autoimmune diseases, including type 1 diabetes, multiple sclerosis, rheumatoid arthritis and inflammatory bowel disease18. Helper T cells play key roles in all these diseases. Thus, understanding VitD biology in helper T cells has potential translational impact.

Our data indicate the complexities of TFs working within networks to regulate sets of genes. After VitD ligates VDR, c-JUN, STAT3 and BACH2 are recruited to acetylated loci, shaping the transcriptional response to VitD. c-JUN is a member of the AP-1 basic leucine zipper family, primarily involved in DNA transcription45. This TF was bound adjacent to 40% of VitD-regulated coding loci. BACH2 is a critical immunoregulatory TF38,39 downregulated in lesional versus non-lesional psoriatic skin46. Active VitD concentrations inversely correlate with severity of psoriasis40. We found that VitD treatment of psoriatic lesional skin upregulated BACH2 expression. Both haploinsufficiency and single nucleotide variants of BACH2 associate with monogenic and polygenic autoimmunity, respectively, in humans36,47. No BACH2 knockout humans have yet been identified, suggesting incompatibility of complete BACH2 deficiency with life. Indeed, Bach2–/– mice succumb to fatal autoimmunity. We found that loss of even 50% of the normal cellular concentration of BACH2 in the haploinsufficient state substantially altered (~70% of) the VitD-regulated transcriptome. As only a proportion of these genes were directly BACH2-bound, it is probable that BACH2 is a requisite for normal recruitment and function of the other transcriptional regulators.

Both the incidence and severity of COVID-19 are epidemiologically associated with VitD deficiency/insufficiency19, but the molecular mechanisms remain unknown. We found a link between the inflammatory TH1 program and a VitD-repressed gene set. Attempts to study CD4+ T cells from the site of inflammation were unsuccessful due to the rapid apoptosis of patient cells, but our in silico analyses suggest either dysregulation of the VitD program in COVID-19 or that simple deficiency/insufficiency of substrate (VitD) might explain the epidemiological association.

IL-6 is a pleiotropic, often pro-inflammatory, cytokine. IL-6 is implicated in the COVID-19 ‘cytokine storm’ and targeting of this cytokine specifically has proved beneficial to patients32. Our data suggest that pro-inflammatory IL-6 functions may be redirected to production of anti-inflammatory IL-10 by VitD in activated human helper T cells. VitD supplementation in children significantly increases serum IL-6 (and nonsignificantly increases IL-10)48 indicating that these observations may also occur in vivo. In the skin, where VitD concentrations are high, IL-6 overexpression protects from injurious stimuli or infection49 and IL-6-deficiency impairs wound healing50. Moreover, an adverse effect of anti-IL-6R for treating inflammatory arthritis is idiosyncratic development of psoriasis51, indicating a tolerogenic role for IL-6 at this site. Thus, adjunct VitD therapy in severe COVID-19 could potentially divert pro-inflammatory and induce anti-inflammatory effects of IL-6, which may be an alternative to blocking IL-6R signaling.

These data identified the VitD pathway as a potential mechanism to accelerate shutdown of TH1 cells in severe COVID-19. From experience in other diseases, it is likely that VitD will be ineffective as monotherapy. Combination therapy could potentially ameliorate significant adverse effects of other drugs, for example high-dose corticosteroids, including over-immunosuppression or metabolic side-effects. An important consideration of VitD therapy in COVID-19 is stimulation of IL-6 production from CD4+ T cells. Although autocrine/paracrine IL-6 induces IL-10 in these cells, IL-6 could potentially have pro-inflammatory properties on other cells. These possibilities may be mitigated by adding VitD as an adjunct to other immunomodulators, such as corticosteroids or JAK inhibitors13. Of note, two randomized clinical trials with calcifediol, a VitD analog with high bioavailability not requiring hepatic 25-hydroxylation, comprising >1,000 patients together, reported reductions in risk of intensive-care unit admission or death when used in addition to standard care (odds ratio of 0.13 and 0.22, respectively52,53). These findings are not necessarily specific to COVID-19, as VitD can protect against acute respiratory tract infections in general17.

In conclusion, we identified an autocrine/paracrine VitD loop permitting TH1 cells to both activate and respond to VitD as part of a shutdown program repressing IFN-γ and enhancing IL-10. These events involved significant epigenetic reshaping and recruitment of a network of key TFs. These pathways could potentially be exploited therapeutically to accelerate the shutdown program of hyper-inflammatory cells in patients with severe COVID-19.

Quote from Wyttenbach

Never heard about Ivermectin and the "India Ziverdo kit". Its a 99.99% insurance much better than vaccines and fights all version of virus.

Since in medicine no treatment is 99.99% effective even without looking at the RCT results you know this is a Wyttenfact. W - why do you do it?

• If you look at the blinded RCT results those that are high quality (e.g. not sloppy methodology allowing hope to triumph over accuracy) show no obvious effect
• If you look at the ongoing large-scale at home RCT tests - no easy to see effect, or they have have stopped the trials with positive interim results.

We can rule out ivermectin having a large effect. Could have some effect? Of course - you can never rule that out.

Quote from Mark U

Huh? It was well known that vaccine efficacy was waning well before Delta arrived on the scene.

Even in the Lancet study that looked at recent household transmission in September, the virus was cleared faster with the Delta infection than pre-Alpha infection in the vaccinated. There was also moderate evidence that Delta infection growth was slowed more that pre-Alpha infection growth in the vaccinated.

https://www.thelancet.com/jour…-3099(21)00648-4/fulltext

Maybe it's time to blame the vaccines for their waning efficacy against infection and transmission, rather than the variants.

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I think you are doing it again mark - biut mainly you are juts blinded by a strong antivaxxer prejudice.

For example looking at fragmentary evidence the virus was cleared faster - that is nothing to do with either efficacy or transmission - the two metrics that matter to people. nor is the speed at which vaccine efficacy wanes.

Both speed of viral clearance and sped at which efficacy wanes are particularly difficult to measure since they are conflated with lots of other factors, which is I guess why you highlight possible evidence.

I am talking about efficacy against infection - where the evidence that it is higher against original (or alpha) than delta is pretty well 100%.

There is a good reason for this - typical initial doses with delta are much higher because it is much more infections (nasal particle loads 1000X). To prevent infection you need neutralising antibody concentration high enough to neutralise - immediately.

In addition lab results tell us that antibody concentration is higher for original than for alpha, and alpha than for delta.

It would be very surprising for anything else to be true, given how specific the antibodies are and the spike mutations between original, alpha and delta.

I guess if you incorporate antivaxxer memes into your worldview, to make them fit you end up with a lot of other strange ideas (like that delta is a much milder disease, against naive individuals) than original COVID. Must be easy to do this if you view all the mainstream data (like that below) as generated by corrupt or incompetent people...

Table 2 Reported impact of SARS-CoV-2 variants on vaccine efficacy and effectiveness

Quote from THHuxleynew

Since in medicine no treatment is 99.99% effective even without looking at the RCT results you know this is a Wyttenfact. W - why do you do it?

• If you look at the blinded RCT results those that are high quality (e.g. not sloppy methodology allowing hope to triumph over accuracy) show no obvious effect
• If you look at the ongoing large-scale at home RCT tests - no easy to see effect, or they have have stopped the trials with positive interim results.

We can rule out ivermectin having a large effect. Could have some effect? Of course - you can never rule that out.

If you become one of the breakthrough infection patients, lips turn blue and need to check in to a hospital...

Given the choice, would you admit yourself to a hospital with a 95.6% COVID treatment success rate knowing they use IVM, or other hospitals that average 79% success and ban it's use?

Merck’s Integrity Sets Example (and Challenge) for Pfizer and Moderna to Report Absolute Risk Reductions

Merck’s Integrity Sets Example (and Challenge) for Pfizer and Moderna to Report Absolute Risk Reductions

Note that views expressed in this opinion article are the writer’s personal views and not necessarily those of TrialSite.Dr. Ron Brown – Opinion Editorial

trialsitenews.com

November 27, 2021

When Merck reported the absolute risk reduction (ARR) of their COVID-19 pill Molnupiravir in their press release on November 26, 2021, the company set an example of integrity, honesty, and transparency that has yet to be matched by Pfizer and Moderna during the COVID-19 pandemic: Merck Update on Results from Study of Molnupiravir. The absolute risk reduction in a clinical trial is the mathematical difference between the event rates in the treatment and placebo groups. In the Merck clinical trials, events were defined as COVID-19 patient hospitalizations and deaths. In the updated analysis reported in the press release, the Molnupiravir rate of hospitalizations and deaths was 6.8% and the placebo rate was 9.7%. That equals a difference of 2.9% or an absolute risk reduction of approximately 3% reported in the press release. The press release also reported the usual relative risk reduction (RRR), which is a bumped-up version of the ARR. The RRR is calculated by dividing the ARR (2.9%) by the placebo event rate (9.7%)—in this case equaling 29.8% or approximately 30%; ten times higher than the ARR!

Both the ARR and RRR should be reported to the public, according to FDA guidelines: Communicating Risks and Benefits: An Evidence Based User’s Guide. However, these guidelines were flagrantly ignored by Pfizer, Moderna, and the FDA’s own Advisory Committee when the ARR was never mentioned during the authorization and approval processes of the COVID-19 mRNA vaccines.

After releasing their updated analysis, Merck took a hit in its stock value: Merck’s update on molnupiravir hits share price. Obviously, reporting the ARR along with a lower treatment event rate has potential negative consequences for the economic return on investment for pharmaceutical companies.

But concealing the ARR also has serious consequences in misleading the public about treatment efficacy.

Challenge to Pfizer and Moderna

What say you, Pfizer and Moderna? Do you have the guts to rise to Merck’s level of honesty and report the ARR of your mRNA vaccines to the public? The challenge is on!

Quote from Fm1

Low genetic diversity may be an Achilles heel of SARS-CoV-2

https://www.pnas.org/content/117/40/24614

Scientists worldwide are racing to develop effective vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID-19 pandemic. An important and perhaps underappreciated aspect of this endeavor is ensuring that the vaccines being developed confer immunity to all viral lineages in the global population. Toward this end, a seminal study published in PNAS (1) analyzes 27,977 SARS-CoV-2 sequences from 84 countries obtained throughout the course of the pandemic to track and characterize the evolution of the novel coronavirus since its origination. The principle conclusion reached by the authors of this work is that SARS-CoV-2 genetic diversity is remarkably low, almost entirely the product of genetic drift, and should not be expected to impede development of a broadly protective vaccine.

Although errors introduced during genome replication are a major source of genetic variation in all virus populations, limiting the fitness costs of accumulated errors is especially critical for coronaviruses, the RNA genomes of which are the largest known. For this reason, coronaviruses evolved nonstructural protein 14 (nsp14), which accompanies viral replicases during RNA synthesis and excises misincorporated ribonucleotides from nascent strands before they can be extended, thus preventing errors from becoming permanent. This error-correcting capacity was unknown among RNA viruses prior to its discovery in SARS-CoV-1 (2, 3), and it contributes to a replication error rate more than 10-fold lower than that of other RNA viruses (4, 5). This activity also likely contributes to the low genetic diversity of SARS-CoV-2, although to our knowledge nsp14 function in the novel coronavirus has yet to be investigated.

For many viruses, surface glycoproteins contain not only elements required for specific binding of cellular receptors, membrane fusion, and virus entry into the host cell but also epitopes recognized by neutralizing antibodies produced as part of an effective adaptive immune response. Hence, tracking genetic variation in the SARS-CoV-2 surface glycoprotein is of paramount importance for determining the likelihood of vaccine effectiveness or immune escape. To put this variation in perspective, Fig. 1 shows a graphical illustration of comparative genetic diversity among surface glycoproteins of select human pathogenic viruses, including SARS-CoV-2, correlated with the availability and effectiveness of respective preventive vaccines.

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Infidelity of SARS-CoV Nsp14-exonuclease mutant virus replication is revealed by complete genome sequencing

Infidelity of SARS-CoV Nsp14-exonuclease mutant virus replication is revealed by complete genome sequencing - PubMed

Most RNA viruses lack the mechanisms to recognize and correct mutations that arise during genome replication, resulting in quasispecies diversity that is…

pubmed.ncbi.nlm.nih.gov

Abstract

Most RNA viruses lack the mechanisms to recognize and correct mutations that arise during genome replication, resulting in quasispecies diversity that is required for pathogenesis and adaptation. However, it is not known how viruses encoding large viral RNA genomes such as the Coronaviridae (26 to 32 kb) balance the requirements for genome stability and quasispecies diversity. Further, the limits of replication infidelity during replication of large RNA genomes and how decreased fidelity impacts virus fitness over time are not known. Our previous work demonstrated that genetic inactivation of the coronavirus exoribonuclease (ExoN) in nonstructural protein 14 (nsp14) of murine hepatitis virus results in a 15-fold decrease in replication fidelity. However, it is not known whether nsp14-ExoN is required for replication fidelity of all coronaviruses, nor the impact of decreased fidelity on genome diversity and fitness during replication and passage. We report here the engineering and recovery of nsp14-ExoN mutant viruses of severe acute respiratory syndrome coronavirus (SARS-CoV) that have stable growth defects and demonstrate a 21-fold increase in mutation frequency during replication in culture. Analysis of complete genome sequences from SARS-ExoN mutant viral clones revealed unique mutation sets in every genome examined from the same round of replication and a total of 100 unique mutations across the genome. Using novel bioinformatic tools and deep sequencing across the full-length genome following 10 population passages in vitro, we demonstrate retention of ExoN mutations and continued increased diversity and mutational load compared to wild-type SARS-CoV. The results define a novel genetic and bioinformatics model for introduction and identification of multi-allelic mutations in replication competent viruses that will be powerful tools for testing the effects of decreased fidelity and increased quasispecies diversity on viral replication, pathogenesis, and evolution.

Quote from Shane D.

If you become one of the breakthrough infection patients, lips turn blue and need to check in to a hospital...

Given the choice, would you admit yourself to a hospital with a 95.6% COVID treatment success rate knowing they use IVM, or other hospitals that average 79% success and ban it's use?

79% for real, or 95.6% W & FLCC kooks?

I'd go for reality any day.

And, for non-kooks, hospital treatment success rate from depends critically on demographic intake, and criteria for admission. We all remember Zelenko's spectacular claims from a 25 years younger than typical US demographic?

Quote from Wyttenbach

Never heard about Ivermectin and the "India Ziverdo kit". Its a 99.99% insurance much better than vaccines and fights all version of virus.

A broad-spectrum antibiotic that is reported to reduce the severity and recovery time of COVID-19 patients: it is not a preventative measure. The evidence is also anecdotal and not from controlled studies. If I had a bad dose of Covid in spite of being innoculated, then I would probably want to give it a go.

Quote from THHuxleynew

The vaccines induce

1. neutralising antibodies preventing infection which alas decays quite quickly.

2. memory so that new neutralising antibodies can be regenerated in response to a new infection more quickly than in an unprotected individual

3. memory T-cell response.

Only 1. prevents infection. 2. & 3. help prevent severe disease.

In addition 1. and 2. are very specific to the spike proteins (1st gen vaccines use only those, and anyway they are better conserved than anything else). 3. is broader in response, and also it seems lasts longer.

So the idea is that for delta, 1. & 2. response is lower, but probably still there. 3. response remains almost as good as for original covid.

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I repeat, in a slightly modified form, what I stated earlier: 'Its a no brainer. Vaccine is humanity's best bet', adding that the inoculation levels need to be in the 80% plus at the double dose level to keep Covid in check. Japan, with the aid of good hygiene and widespread use of masks, achieved control at a far lower inoculation rate, as flagged in Alan Smith's earlier post.

Quote from Alan Smith

What's behind the rapid disappearance of the delta variant in Japan? It could be self-extinction. Many scholars point to a variety of explanations for the sudden end of the fifth wave, but one research group says the coronavirus variant may have actually… http://www.japantimes.co.jp

The best thing anyone can do for themselves, their loved ones and their communities to reduce the affects of the Covid scourge, is to get the virtually painless two jabs, and so increase the community inoculation levels.

Quote from THHuxleynew

Must be easy to do this if you view all the mainstream data (like that below) as generated by corrupt or incompetent people...

That data is nothing new! Newer variants tend to me more transmissible, and the vaccines thus tend to be less effective at preventing transmission with the new variants. No surprise there. My point is, that decrease in effectiveness against different strains pales in comparison to the vaccine's inherent decline in effectiveness over time irregardless of the strain.

Let's direct the description of incompetence or corruption to where it is due : To those 'health' officials who, despite the data that the vaccine becomes almost useless against infection and transmission over time, are nevertheless still pushing for vaccine passports and mandates and boosters. They are pushing for exactly the narrative that big pharma wants, and big media has very effectively sold it to the public. Too bad the pubic didn't have more immunity to propaganda.

Tomorrow the citizens of Switzerland will take an extraordinary measure and vote on mandatory vaccine passes. We will soon see how immune they really are to fear and propaganda.