Covid Vaccine

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According to a study that examined how informed consent is given to COVID-nineteen vaccine trial participants, disclosure forms fail to inform volunteers that the vaccine might make them susceptible to more severe illness if they're exposed to the virus.

The study,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Run a risk of COVID-nineteen Vaccine Worsening Clinical Disease," published in the International Journal of Clinical Practise, October 28, 2020, points out that "COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated."

"Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the evolution and testing of these vaccines propose a serious mechanistic business: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), exist they composed of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-nineteen illness via antibody-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 adequate patient comprehension of this gamble is unlikely to occur, obviating truly informed consent by subjects in these trials.
The specific and pregnant COVID-nineteen risk of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well as those being recruited for the trials and future patients later on vaccine approval, in society to meet the medical ethics standard of patient comprehension for informed consent."


What Is Antibody-Dependent Enhancement?

Every bit noted by the authors of that International Journal of Clinical Do paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious concern: The vaccines have a trend to trigger antibody-dependent enhancement.

What exactly does that hateful? In a nutshell, it ways that rather than heighten your amnesty against the infection, the vaccine actually enhances the virus' power to enter and infect your cells, resulting in more severe disease than had you not been vaccinated. ii

This is the exact opposite of what a vaccine is supposed to do, and a significant problem that has been pointed out from the very showtime of this push for a COVID-xix vaccine. The 2003 review paper "Antibiotic-Dependent Enhancement of Virus Infection and Disease" explains it this way:iii

"In general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This action is known as antibody-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 health 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 get a great business concern 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 development, which began in 2002, following iii consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had virtually xxx promising candidates.

Of those, the four all-time vaccine candidates were so given to ferrets, which are the closest analogue to human lung infections. In the video below, which is a select outtake from my full interview, Kennedy explains what happened side by side. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, in one case 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 affliction that is very similar to that caused past coronaviruses. At that fourth dimension, they had decided to skip beast trials and go direct to human trials.

"They tested it on I think well-nigh 35 children, and the same thing happened," Kennedy said. "The children developed a champion antibiotic response — robust, durable. It looked perfect [but when] the children were exposed to the wild virus, they all became sick. Two of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH."


Neutralizing Versus Binding Antibodies

Coronaviruses produce not only one but two dissimilar types of antibodies:

  • Neutralizing antibodies,4 besides referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodiesv (also known as non-neutralizing antibodies) that cannot foreclose viral infection

Instead of preventing viral infection, bounden antibodies trigger an abnormal allowed response known as "paradoxical immune enhancement." Another fashion to wait at this is your allowed organization is actually backfiring and not functioning to protect you just actually making you worse.

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to brand the SARS-CoV-two fasten poly peptide (South protein). The spike poly peptide, which is what attaches to the ACE2 receptor of the cell, is the kickoff stage of the ii-stage procedure viruses use to gain entry into cells.

The thought is that by creating the SARS-CoV-ii fasten poly peptide, your immune system will commence production of antibodies, without making y'all sick in the process. The fundamental question is, which of the ii types of antibodies are being produced through this process?


Without Neutralizing Antibodies, Await More than Severe Affliction

In an April 2020 Twitter thread,six The Immunologist noted: "While developing vaccines ... and because amnesty passports, we must first sympathise the complex role of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that take raised concerns about ADE.

The first is a 2017 study7 in PLOS Pathogens, "Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absence 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. (Meaning, once you recover from a viral infection, say measles, you're immune and won't contract the illness again.)

To make up one's mind how MERS affects the allowed system, the researchers infected white rabbits with the virus. The rabbits got sick and developed antibodies, but those antibodies were non the neutralizing kind, meaning 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 increment in viral RNA titers," the authors noted. Interestingly, neutralizing antibodies were elicited during this second infection, preventing the animals from existence infected a third fourth dimension. According to the authors:

"Our information from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung illness on re-exposure to MERS-CoV."

In other words, if the vaccine does not result in a robust response in neutralizing antibodies, y'all might be at chance for more severe lung disease if you're infected with the virus.

And hither'southward an important indicate: COVID-xix vaccines are Non designed to forestall infection. As detailed in "How COVID-19 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 besides known to cause ADE. Equally explained in a Swiss Medical Weekly paper published in April 2020:8

"The pathogenesis of COVID-19 is currently believed to proceed via both straight cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent damage may involve the so-called antibody-dependent enhancement (ADE).
ADE is a very well-known cascade of events whereby viruses may infect susceptible cells via interaction between 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 non only for the agreement of viral pathogenesis, but also for developing antiviral strategies, notably vaccines ...
In that location are iv serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may last only upwards to ii years.
In Dengue fever, reinfection with a different serotype runs a more than astringent class when the protective antibody titer wanes. Here, non-neutralizing antibodies take 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 unlike from the first infection.
Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the college the titer of such antibodies post-obit 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 rate for Dengue among vaccinated children under the age of nine was greater than the charge per unit amid 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 protein 1 immunoglobulin 1000 (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-type infection from those following vaccination, showed that the vaccine was able to protect against astringent Dengue [in] those who had been exposed to the natural infection before vaccination, and that the hazard of severe clinical outcome was increased amid seronegative persons.
Based on this, a Strategic Advisor Grouping of Experts convened by Globe Health Organization (WHO) ended that only Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could stop up being important for the COVID-nineteen vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is too caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually be at increased hazard for severe COVID-xix after vaccination, and simply those who have already recovered from a bout of COVID-xix would be protected against severe affliction past the vaccine.

To be clear, we exercise not know whether that is the case or non, but these are important areas of inquiry and the current vaccine trials volition but not exist able to answer this important question.

The Swiss Medical Weekly paper 9 also reviews the evidence of ADE in coronavirus infections, citing research showing inoculating cats against 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 paper too cites inquiry 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 past Antibodies Against Spike Proteins," published in 2014, establish 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 higher levels of apoptosis.

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

Combined, our results propose that antibodies against SARS-CoV spike proteins may trigger ADE effects. The data raise new questions regarding a potential SARS-CoV vaccine ..."

A written report11 that ties into this was published in the journal JCI Insight in 2019. Here, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike protein ended up with more astringent 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 impairment, probable by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection After Challenge With SARS-CoV

An interesting 2012 paper 12 with the telling title, "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus," demonstrates what many researchers now fearfulness, namely that COVID-19 vaccines may end up making people more prone to severe SARS-CoV-2 infection.

The newspaper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus. Every bit noted by the authors: xiii

Inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-blazon 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 institute the aforementioned immunopathologic reaction in animals given Southward protein vaccine only, although it appeared to be of bottom intensity.

Thus, a Th2-type immunopathologic reaction on claiming of vaccinated animals has occurred in 3 of four animate being models (not in hamsters) including two different inbred mouse strains with four dissimilar types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine training that does not induce this result 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 take been conducted and reported to induce antibiotic responses and to be 'safe.' However, the evidence for safe is for a curt catamenia of observation.

The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional condom concerns relate to effectiveness and safety against antigenic variants of SARS-CoV and for rubber of vaccinated persons exposed to other coronaviruses, particularly those of the type two group."


The Elderly Are Well-nigh Vulnerable to ADE

On top of all of these concerns, at that place's evidence showing the elderly — who are about vulnerable to severe COVID-19 — are likewise the nearly vulnerable to ADE. Preliminary research findings14 posted on the preprint server medRxiv at the stop of March 2020 reported that middle-anile and elderly COVID-19 patients take far college levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.


Immune Enhancement Is a Serious Business organisation

Another paper worth mentioning is the May 2020 mini reviewfifteen "Affect of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development." As in many other papers, the authors point out that:sixteen

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-two are promising, they both pose a common theoretical rubber concern. Experimental studies take suggested the possibility of immune-enhanced illness of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection ...
Allowed enhancement of affliction can theoretically occur in two ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-ii infection into target cells.
Secondly, antibodies could enhance inflammation and hence severity of pulmonary illness. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. i ...
Currently, in that location are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early on phase clinical trials. Animal studies on these CoVs have shown that the fasten (South) protein-based vaccines (specifically the receptor bounden domain, RBD) are highly immunogenic and protective against wild-type CoV challenge.
Vaccines that target other parts of the virus, such as the nucleocapsid, without the S poly peptide, have shown no protection against CoV infection and increased lung pathology. However, immunization with some S poly peptide based CoV vaccines take also displayed signs of enhanced lung pathology post-obit challenge.
Hence, as well the selection of antigen target, vaccine efficacy and risk 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

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


Do a Gamble-Benefit Assay Earlier Making Upwardly Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end up being, they'll be released to the public in relatively brusque lodge. Nearly predict one or more vaccines will be ready sometime in 2021.

Ironically, the information 17,18,xix we at present have no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60. xx If you're under the age of 40, your hazard of dying from COVID-xix is merely 0.01%, meaning you accept a 99.99% risk of surviving the infection. And yous could ameliorate that to 99.999% if you're metabolically flexible and vitamin D replete.

So, actually, what are we protecting confronting with a COVID-nineteen vaccine? As mentioned, the vaccines aren't even designed to foreclose infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker in one case y'all're exposed to the virus. That seems like a lot of take chances for a truly questionable do good.

To circle back to where nosotros started, participants in current COVID-nineteen vaccine trials are non being told of this risk — that by getting the vaccine they may end upwardly with more severe COVID-19 one time they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

In closing, consider what this PNAS news feature states almost the gamble of vaccine-induced immune enhancement and dysfunction, specially for the elderly, the very people who would need the protection a vaccine might offer the almost:21

"Since the 1960s, tests of vaccine candidates for diseases such every bit dengue, respiratory syncytial virus (RSV), and severe astute respiratory syndrome (SARS) have shown a paradoxical phenomenon:
Some animals or people who received the vaccine and were later exposed to the virus developed more astringent disease than those who had not been vaccinated. The vaccine-primed immune system, in certain cases, seemed to launch a shoddy response to the natural infection ...
This allowed backfiring, or so-called immune enhancement, may manifest in unlike ways such equally 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 fence that although ADE has received the most attention to date, information technology is less probable than the other immune 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 trouble is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and good in coronaviruses ... at the Academy of N Carolina at Chapel Hill.
In previous studies of SARS, anile mice were institute to have particularly high risks of life-threatening Th2 immunopathology ... in which a faulty T cell response triggers allergic inflammation, and poorly functional antibodies that form immune complexes, activating the complement system and potentially damaging the airways."


Sources and References

  • 1 International Periodical of Clinical Practice, October 28, 2020 DOI: ten.111/ijcp.13795
  • 2, 21 PNAS.org April xiv, 2020 117 (fifteen) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • iv Scientific discipline Direct Neutralizing Antibody
  • 5 Science Direct Binding Antibiotic
  • six Twitter, The Immunologist Apr 9, 2020
  • 7 PLOS Pathogens 2017 Aug; xiii(8): e1006565
  • viii, 9 Swiss Medical Weekly Apr 16, 2020; 150:w20249
  • ten Biochemical and Biophysical Research Communications Baronial 22, 2014; 451(2): 208-214
  • 11 JCI Insight Feb 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS I April 2012; 7(4): e35421 (PDF)
  • 13 PLOS ONE April 2012; 7(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:ten.1101/2020.03.thirty.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • sixteen EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September 2, 2020 DOI: 10.7326/M20-5352
  • xviii YouTube, SARS-CoV-two and the rise of medical technocracy, Lee Merritt, Doc, aprox viii minutes in (Prevarication No. ane: Death Risk)
  • 19 Technical Report June 2020 DOI: 10.13140/RG.two.24350.77125