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According to a study that examined how informed consent is given to COVID-19 vaccine trial participants, disclosure forms neglect to inform volunteers that the vaccine might make them susceptible to more than severe disease if they’re exposed to the virus.

The study,1
“Informed Consent Disclosure to Vaccine Trial Subjects of Take a chance of COVID-19 Vaccine Worsening Clinical Illness,” published in the
International Journal of Clinical Do, Oct 28, 2020, points out that “COVID-xix vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were non vaccinated.”

“Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the evolution and testing of these vaccines suggest a serious mechanistic concern: that
vaccines designed empirically using the traditional approach
(consisting of the unmodified or minimally modified coronavirus viral fasten to elicit neutralizing antibodies),
be they composed of protein, viral vector, Dna or RNA and irrespective of delivery method, may worsen COVID-xix disease via antibiotic-dependent enhancement (ADE),” the paper states.

“This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 vaccine trials
that acceptable patient comprehension of this adventure is unlikely to occur, obviating truly informed consent by subjects in these trials.

The specific and pregnant
COVID-nineteen risk of ADE should accept been and should be prominently and independently disclosed to research subjects currently in vaccine trials,
as well equally those beingness recruited for the trials and future patients afterward vaccine approval,
in order to run across the medical ethics standard of patient comprehension for informed consent.”



What Is Antibody-Dependent Enhancement?

As noted past the authors of that
International Journal of Clinical Practice
paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle Due east respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious business organization:
The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that mean? In a nutshell,
it ways that rather than enhance your immunity against the infection, the vaccine really enhances the virus’ ability to enter and infect your cells, resulting in more severe disease than had you lot non been vaccinated.
2

This is the exact opposite of what a vaccine is supposed to do, and a pregnant problem that has been pointed out from the very kickoff of this push button for a COVID-nineteen vaccine. The 2003 review paper “Antibody-Dependent Enhancement of Virus Infection and Disease” explains it this mode:3

“In general, virus-specific antibodies are considered antiviral and play an important function in the control of virus infections in a number of ways. Even so,
in some instances, the presence of specific antibodies can be beneficial to the virus. This activeness is known equally antibiotic-dependent enhancement (ADE) of virus infection.

The ADE of virus infection is
a phenomenon in which virus-specific antibodies enhance the entry of virus, and in some cases the replication of virus,
into monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors.

This phenomenon has been reported in vitro and in vivo for viruses representing numerous families and genera of public wellness and veterinarian importance. These viruses share some mutual features such as preferential replication in macrophages, ability to establish persistence, and antigenic multifariousness.
For some viruses, ADE of infection has go a neat business organization to affliction control by vaccination.”




Previous Coronavirus Vaccine Efforts Have All Failed

In my May 2020 interview higher up with Robert Kennedy Jr., he summarized the history of coronavirus vaccine evolution, which began in 2002, post-obit iii consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine evolution, and had about xxx promising candidates.

Of those, the four all-time vaccine candidates were then given to ferrets, which are the closest analogue to human being lung infections. In the video beneath, which is a select outtake from my total interview, Kennedy explains what happened side by side.
While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, once they were challenged with the wild virus, they all became severely ill and died.

The same thing happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory disease that is very similar to that acquired by coronaviruses. At that time, they had decided to skip beast trials and get straight to man trials.

“They tested it on I think almost 35 children, and the same thing happened,”

Kennedy said.

“The children developed a champion antibody response — robust, durable. It looked perfect [but when] the children were exposed to the wild virus, they all became ill. Two of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH.”



Neutralizing Versus Bounden Antibodies

Coronaviruses produce not just i only two different types of antibodies:

  • Neutralizing antibodies,iv
    besides referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodies5
    (also known every bit not-neutralizing antibodies) that cannot foreclose viral infection

Instead of preventing viral infection, binding antibodies trigger an abnormal allowed response known equally “paradoxical immune enhancement.”
Some other way to look at this is your immune system is really backfiring and not functioning to protect you just actually making you worse.

Many of the COVID-xix vaccines currently in the running are
using mRNA to instruct your cells to make the SARS-CoV-2 spike protein
(S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the kickoff stage of the two-stage process viruses utilise to proceeds entry into cells.

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The idea is that by creating the SARS-CoV-2 fasten protein, your immune system will commence production of antibodies, without making you sick in the procedure. The key question is, which of the two types of antibodies are beingness produced through this process?




Without Neutralizing Antibodies, Await More Severe Illness

In an April 2020 Twitter thread,6
The Immunologist
noted: “While developing vaccines … and because immunity passports, we must first understand the circuitous part of antibodies in SARS, MERS and COVID-19.” He goes on to listing several coronavirus vaccine studies that have raised concerns about ADE.

The kickoff is a 2017 reportseven
in
PLOS Pathogens, “Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absenteeism of Neutralizing Antibody,” which investigated whether
getting infected with MERS would protect the subject against reinfection, as is typically the case with many viral illnesses.
(Significant, once you recover from a viral infection, say measles, yous’re immune and won’t contract the illness again.)

To determine how MERS affects the immune organisation,
the researchers infected white rabbits with the virus.
The rabbits got ill and
developed antibodies, but those antibodies were not the neutralizing kind, pregnant the kind of antibodies that block infection. As a result, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill again, and more severely so.

“In fact,
reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers,” the authors noted. Interestingly, neutralizing antibodies were elicited during this second infection, preventing the animals from being infected a third time. According to the authors:

“Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibiotic titers take waned, may be at take chances for astringent lung disease on re-exposure to MERS-CoV.”

In other words, if the vaccine does not result in a robust response in neutralizing antibodies, you might be at risk for more severe lung illness if you’re infected with the virus.

And here’s an important betoken: COVID-19 vaccines are Non designed to preclude infection. Every bit detailed in “How COVID-xix Vaccine Trials Are Rigged,” a “successful” vaccine merely needs to reduce the severity of the symptoms. They’re not even looking at reducing infection, hospitalization or death rates.


ADE in Dengue Infections

The Dengue virus is as well known to crusade ADE. Equally explained in a
Swiss Medical
Weekly paper published in April 2020:8

“The pathogenesis of COVID-19 is currently believed to keep via both straight cytotoxic and immune-mediated mechanisms. An boosted mechanism facilitating viral prison cell entry and subsequent damage may involve the and then-called antibiotic-dependent enhancement (ADE).

ADE is a very well-known cascade of events whereby viruses may infect susceptible cells
via interaction betwixt virions complexed with antibodies or complement components and, respectively, Fc or complement receptors,
leading to the amplification of their replication.

This phenomenon is of enormous relevance not only for the agreement of viral pathogenesis, but also for developing antiviral strategies, notably vaccines …

There are four serotypes of Dengue virus, all eliciting protective immunity. Nonetheless, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may terminal only up to 2 years.

In Dengue fever,
reinfection with a different serotype runs a more than severe course when the protective antibody titer wanes. Here, not-neutralizing antibodies have over neutralizing ones, bind to Dengue virions, and these complexes mediate the infection of phagocytic cells via interaction with the Fc receptor, in a typical ADE.

In other words, heterotypic antibodies at subneutralizing titres account for ADE in persons infected with a serotype of Dengue virus that is dissimilar from the first infection.

Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the chief infection, the longer the delay to symptomatic secondary infection …”

The paper goes on to detail results from follow-up investigations into the Dengue vaccine, which revealed
the hospitalization charge per unit for Dengue among vaccinated children under the historic period of ix was greater than the charge per unit among controls.
The explanation for this appears to be that the vaccine mimicked a primary infection, and as that immunity waned, the children became susceptible to ADE when they encountered the virus a second time.
The author explains:

“A post hoc analysis of efficacy trials, using an anti-nonstructural poly peptide 1 immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-blazon infection from those post-obit vaccination, showed that the vaccine was able to protect confronting severe Dengue [in] those who had been exposed to the natural infection before vaccination, and that the chance of severe clinical outcome was increased amongst seronegative persons.

Based on this, a
Strategic Advisor Grouping of Experts
convened by
World Health Organization
(WHO) concluded that only Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination.”


ADE in Coronavirus Infections

This could end up being important for the COVID-19 vaccine. Hypothetically speaking,
if SARS-CoV-2 works like Dengue, which is as well caused by an RNA virus, and then anyone who has non tested positive for SARS-CoV-two might actually exist at increased run a risk for severe COVID-19 subsequently vaccination, and only those who have already recovered from a bout of COVID-xix would be protected against severe illness by the vaccine.

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To be clear, we do not know whether that is the example or not, just these are important areas of inquiry and the electric current vaccine trials will simply not be able to answer this important question.

The Swiss Medical Weekly paper
9
too reviews the evidence of ADE in coronavirus infections, citing research showing inoculating cats confronting the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the disease when challenged with the same FIPV serotype as that in the vaccine.

Experiments have shown immunization with a diverseness of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The newspaper also cites enquiry showing
“Antibodies elicited by a SARS-CoV vaccine enhanced infection of B cell lines in spite of protective responses in the hamster model.”
Another paper,ten
“Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins,” published in 2014, constitute that:

“… higher concentrations of anti-sera against SARS-CoV neutralized SARS-CoV infection, while highly diluted anti-sera significantly increased SARS-CoV infection and induced college levels of apoptosis.

Results from infectivity assays indicate that SARS-CoV ADE is primarily mediated by diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. Nosotros also generated monoclonal antibodies confronting SARS-CoV fasten proteins and observed that near of them promoted SARS-CoV infection.

Combined,
our results suggest that antibodies against SARS-CoV fasten proteins may trigger ADE effects. The data enhance new questions regarding a potential SARS-CoV vaccine …”

A study11
that ties into this was published in the periodical
JCI Insight
in 2019.
Here, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike poly peptide ended up with more severe lung pathology when the animals were exposed to the SARS virus.
And, when they transferred anti-spike IgG antibodies into unvaccinated macaques, they developed acute diffuse alveolar damage, likely by “skewing the inflammation-resolving response.”


SARS Vaccine Worsens Infection After Claiming With SARS-CoV

An interesting 2012 paper

12


with the telling title, “Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Claiming with the SARS Virus,” demonstrates what many researchers now fear, namely that COVID-19 vaccines may end upwards making people more prone to astringent SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a diversity of SARS vaccines resulted in pulmonary immunopathology one time challenged with the SARS virus. As noted by the authors:

13

Inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-type immunopathologic in lungs after challenge.

As indicated, 2 reports attributed the immunopathology to presence of the Due north poly peptide in the vaccine; however, we found the aforementioned immunopathologic reaction in animals given Due south protein vaccine only, although it appeared to be of bottom intensity.

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in iii of four animal models (not in hamsters) including ii different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine grooming that does not induce this consequence in mice, ferrets and nonhuman primates has not been reported.

This combined experience provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines accept been conducted and reported to induce antibody responses and to be ‘safe.’ Withal, the evidence for safety is for a curt period of ascertainment.

The concern arising from the present written report is for an immunopathologic reaction occurring amongst vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional rubber concerns relate to effectiveness and rubber confronting antigenic variants of SARS-CoV and for prophylactic of vaccinated persons exposed to other coronaviruses, particularly those of the type 2 group.”




The Elderly Are Nearly Vulnerable to ADE

On top of all of these concerns, there’s bear witness showing the elderly — who are almost vulnerable to severe COVID-xix — are also the well-nigh vulnerable to ADE. Preliminary research findings14
posted on the preprint server
medRxiv
at the end of March 2020 reported that middle-aged and
elderly COVID-nineteen patients have far higher levels of anti-fasten antibodies — which, again, increase infectivity — than younger patients.




Immune Enhancement Is a Serious Concern

Another paper worth mentioning is the May 2020 mini review15
“Touch on of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Evolution.” As in many other papers, the authors point out that:16

“While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-ii are promising, they both pose a mutual theoretical safe business. Experimental studies have suggested the possibility of immune-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection …

Immune enhancement of disease can theoretically occur in 2 ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-2 infection into target cells.

Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. one …

Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early on stage clinical trials. Animal studies on these CoVs accept shown that the spike (Southward) protein-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective against wild-blazon CoV challenge.

Vaccines that target other parts of the virus, such as the nucleocapsid, without the S protein, have shown no protection against CoV infection and increased lung pathology. Withal, immunization with some South protein based CoV vaccines have too displayed signs of enhanced lung pathology following challenge.

Hence, besides the choice of antigen target, vaccine efficacy and take chances of immunopathology may be dependent on other ancillary factors, including adjuvant formulation, historic period at vaccination … and route of immunization.”

mechanism-of-ade-and-antibody-mediated-immunopathology

© manufactures.mercola.com

Figure 1: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune circuitous internalization is mediated by the engagement of activating Fc receptors on the cell surface. Co-ligation of inhibitory receptors so results in the inhibition of antiviral responses which leads to increased viral replication. Correct panel: Antibodies tin can cause immunopathology past activating the complement pathway or antibody-dependent cellular cytotoxicity (ADCC). For both pathways, excessive immune activation results in the release of cytokines and chemokines, leading to enhanced affliction pathology.

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Do a Risk-Benefit Analysis Before Making Up Your Mind

In all likelihood, regardless of how constructive (or ineffective) the COVID-19 vaccines stop upward beingness, they’ll exist released to the public in relatively short order. Most predict 1 or more than vaccines will be prepare sometime in 2021.


Ironically, the data



17,18,xix




we now take no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those nether the age of 60.




20




If yous’re under the age of 40, your risk of dying from COVID-xix is merely 0.01%, pregnant you have a 99.99% risk of surviving the infection. And you lot could ameliorate that to 99.999% if you lot’re metabolically flexible and vitamin D replete.

And then, really, what are we protecting confronting with a COVID-xix vaccine? As mentioned, the vaccines aren’t fifty-fifty designed to prevent infection, simply reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you’re exposed to the virus. That seems like a lot of chance for a truly questionable do good.

To circle back to where we started, participants in current COVID-nineteen vaccine trials are non being told of this risk — that by getting the vaccine they may stop upwardly with more astringent COVID-xix one time they’re infected with the virus.




Lethal Th2 Immunopathology Is Another Potential Take a chance

In endmost, consider what this
PNAS news
feature states about the adventure of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offer the most:21

“Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) have shown a paradoxical miracle:

Some animals or people who received the vaccine and were afterwards exposed to the virus developed more severe disease than those who had non been vaccinated.

The vaccine-primed immune arrangement, in certain cases, seemed to launch a shoddy response to the natural infection …

This immune backfiring, or then-called immune enhancement, may manifest in different ways such as antibody-dependent enhancement (ADE), a procedure in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation acquired by Th2 immunopathology. In some cases, the enhancement processes might overlap …

Some researchers debate that although ADE has received the most attention to appointment, it is less likely than the other allowed enhancement pathways to cause a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its behavior in the man trunk.

‘There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,’ says Ralph Baric, an epidemiologist and expert in coronaviruses … at the University of Due north Carolina at Chapel Hill.


In previous studies of SARS, anile mice were found to have particularly loftier risks of life-threatening Th2 immunopathology … in which a faulty T cell response triggers allergic inflammation, and poorly functional antibodies that course immune complexes, activating the complement system and potentially dissentious the airways.”




Sources and References

  • 1 International Journal of Clinical Exercise, October 28, 2020 DOI: x.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
  • three Viral Immunology 2003;16(i):69-86
  • iv Scientific discipline Direct Neutralizing Antibody
  • 5 Science Direct Binding Antibiotic
  • 6 Twitter, The Immunologist April nine, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(eight): e1006565
  • eight, ix Swiss Medical Weekly April xvi, 2020; 150:w20249
  • 10 Biochemical and Biophysical Enquiry Communications Baronial 22, 2014; 451(2): 208-214
  • 11 JCI Insight Feb 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE April 2012; 7(four): e35421 (PDF)
  • xiii PLOS ONE April 2012; seven(iv): e35421 (PDF), page 11
  • 14 medRxiv DOI:ten.1101/2020.03.30.20047365 (PDF)
  • xv EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September two, 2020 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the ascension of medical technocracy, Lee Merritt, Physician, aprox 8 minutes in (Lie No. i: Death Run a risk)
  • 19 Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125

Source: https://www.sott.net/article/445095-How-COVID-19-vaccine-can-destroy-your-immune-system