Covid Vaccine

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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,one "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Affliction," published in the International Periodical of Clinical Practice, 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 take never been approved, and the data generated in the evolution and testing of these vaccines suggest a serious mechanistic business concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to arm-twist neutralizing antibodies), be they equanimous of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibiotic-dependent enhancement (ADE)," the paper states.
"This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-xix vaccine trials that adequate patient comprehension of this risk is unlikely to occur, obviating truly informed consent past subjects in these trials.
The specific and significant COVID-19 risk of ADE should have been and should be prominently and independently disclosed to inquiry subjects currently in vaccine trials, as well as those existence recruited for the trials and futurity patients after vaccine approval, in guild to run into the medical ideals standard of patient comprehension for informed consent."


What Is Antibody-Dependent Enhancement?

Equally noted by the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for astringent acute respiratory syndrome coronavirus (SARS-CoV), Centre E respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious concern: The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that mean? In a nutshell, information technology means 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 affliction than had yous not been vaccinated. ii

This is the exact opposite of what a vaccine is supposed to practise, and a meaning problem that has been pointed out from the very beginning of this push for a COVID-19 vaccine. The 2003 review newspaper "Antibody-Dependent Enhancement of Virus Infection and Illness" explains information technology this mode:three

"In full general, virus-specific antibodies are considered antiviral and play an of import office in the command of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This activity is known as 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 health and veterinary importance. These viruses share some common features such as preferential replication in macrophages, power to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a great business concern to disease control by vaccination."


Previous Coronavirus Vaccine Efforts Have All Failed

In my May 2020 interview above with Robert Kennedy Jr., he summarized the history of coronavirus vaccine development, which began in 2002, following three consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had about xxx promising candidates.

Of those, the iv best vaccine candidates were and so given to ferrets, which are the closest counterpart to human lung infections. In the video below, which is a select outtake from my total interview, Kennedy explains what happened next. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, one time 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 illness that is very similar to that acquired by coronaviruses. At that time, they had decided to skip animal trials and go directly to homo trials.

"They tested it on I think near 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. 2 of them died. They abandoned the vaccine. Information technology was a big embarrassment to FDA and NIH."


Neutralizing Versus Binding Antibodies

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

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

Instead of preventing viral infection, binding antibodies trigger an aberrant immune response known equally "paradoxical allowed enhancement." Another style to look at this is your immune system is really backfiring and not functioning to protect you but really making you worse.

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to make the SARS-CoV-ii spike poly peptide (S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the commencement stage of the two-stage process viruses use to proceeds entry into cells.

The idea is that by creating the SARS-CoV-two fasten poly peptide, your allowed system will commence production of antibodies, without making y'all sick in the procedure. The key question is, which of the 2 types of antibodies are existence produced through this process?


Without Neutralizing Antibodies, Expect More than Severe Illness

In an April 2020 Twitter thread,half dozen The Immunologist noted: "While developing vaccines ... and considering immunity passports, we must first understand the complex role of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that have raised concerns almost ADE.

The first is a 2017 written 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, you're immune and won't contract the illness once again.)

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

"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 data from the rabbit model suggests that people exposed to MERS-CoV who neglect to develop a neutralizing antibiotic response, or persons whose neutralizing antibody titers accept waned, may be at risk for astringent lung disease on re-exposure to MERS-CoV."

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

And hither's an of import point: COVID-19 vaccines are Not designed to prevent 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 decease rates.

ADE in Dengue Infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly paper published in April 2020:eight

"The pathogenesis of COVID-nineteen is currently believed to proceed via both straight cytotoxic and allowed-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 distension of their replication.
This phenomenon is of enormous relevance not only for the understanding of viral pathogenesis, but also for developing antiviral strategies, notably vaccines ...
In that location are 4 serotypes of Dengue virus, all eliciting protective amnesty. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against unlike serotypes are short-lived and may last just up to 2 years.
In Dengue fever, reinfection with a dissimilar serotype runs a more severe course when the protective antibody titer wanes. Here, not-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 following the primary 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 nether the historic period of 9 was greater than the rate 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 2nd time. The author explains:

"A post hoc analysis of efficacy trials, using an anti-nonstructural protein 1 immunoglobulin G (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 confronting severe Dengue [in] those who had been exposed to the natural infection before vaccination, and that the risk of severe clinical outcome was increased amongst seronegative persons.
Based on this, a Strategic Counselor Grouping of Experts convened by Earth Wellness Organization (WHO) concluded that only Dengue seropositive persons should exist vaccinated whenever Dengue command programs are planned that include vaccination."

ADE in Coronavirus Infections

This could finish upwards beingness important for the COVID-xix vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually be at increased risk for astringent COVID-nineteen after vaccination, and only those who have already recovered from a bout of COVID-19 would be protected against severe affliction by the vaccine.

To exist clear, we do not know whether that is the case or not, but these are important areas of inquiry and the current vaccine trials volition simply not be able to answer this of import 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 take shown immunization with a variety of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The paper as well cites research showing "Antibodies elicited by a SARS-CoV vaccine enhanced infection of B cell lines in spite of protective responses in the hamster model." Another newspaper,10 "Antibiotic-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins," published in 2014, found that:

"... college 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 bespeak that SARS-CoV ADE is primarily mediated past diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. Nosotros too generated monoclonal antibodies confronting SARS-CoV spike proteins and observed that most 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 journal JCI Insight in 2019. Hither, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike protein concluded upwardly with more severe lung pathology when the animals were exposed to the SARS virus. And, when they transferred anti-fasten IgG antibodies into unvaccinated macaques, they developed astute diffuse alveolar damage, likely past "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Subsequently 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 fear, namely that COVID-xix vaccines may terminate upward making people more decumbent 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. Every bit 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 afterwards challenge.

As indicated, two reports attributed the immunopathology to presence of the N poly peptide in the vaccine; nonetheless, nosotros establish the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity.

Thus, a Th2-blazon immunopathologic reaction on challenge of vaccinated animals has occurred in iii of iv animal models (non in hamsters) including 2 different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine preparation that does not induce this issue 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.' However, the prove for safe is for a short period 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 ground for developing a vaccine for SARS. Additional safety 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 2 group."


The Elderly Are Almost Vulnerable to ADE

On top of all of these concerns, there's prove showing the elderly — who are near vulnerable to severe COVID-19 — are also the virtually vulnerable to ADE. Preliminary research findings14 posted on the preprint server medRxiv at the end of March 2020 reported that center-aged and elderly COVID-nineteen patients have far higher levels of anti-spike antibodies — which, once again, increase infectivity — than younger patients.


Allowed Enhancement Is a Serious Business

Some other paper worth mentioning is the May 2020 mini review15 "Bear upon of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Evolution." As in many other papers, the authors point out that:sixteen

"While evolution of both hyperimmune globulin therapy and vaccine against SARS-CoV-ii are promising, they both pose a mutual theoretical condom concern. Experimental studies have suggested the possibility of allowed-enhanced illness of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-two infection ...
Immune enhancement of disease can theoretically occur in two ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can raise SARS-CoV-2 infection into target cells.
Secondly, antibodies could raise inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. 1 ...
Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animal studies on these CoVs have shown that the spike (Due south) protein-based vaccines (specifically the receptor binding 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 protein, have shown no protection against CoV infection and increased lung pathology. Yet, immunization with some Southward protein based CoV vaccines have too displayed signs of enhanced lung pathology following challenge.
Hence, besides the choice of antigen target, vaccine efficacy and risk of immunopathology may exist dependent on other ancillary factors, including adjuvant formulation, age at vaccination ... and road of immunization."

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

© articles.mercola.com
Effigy 1: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex 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 can crusade immunopathology by 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 illness pathology.


Exercise a Take chances-Do good Analysis Before Making Up Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-xix vaccines end up being, they'll exist released to the public in relatively short order. Most predict one or more than vaccines will be set sometime in 2021.

Ironically, the data 17,eighteen,xix nosotros now accept no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the historic period of 60. 20 If you're under the historic period of forty, your adventure of dying from COVID-19 is just 0.01%, meaning you have a 99.99% chance of surviving the infection. And you could improve that to 99.999% if you're metabolically flexible and vitamin D replete.

So, really, what are nosotros protecting confronting with a COVID-xix vaccine? As mentioned, the vaccines aren't fifty-fifty designed to forestall infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker one time you lot're exposed to the virus. That seems like a lot of risk for a truly questionable benefit.

To circle back to where nosotros started, participants in electric current COVID-nineteen vaccine trials are not being told of this risk — that past getting the vaccine they may stop upward with more than severe COVID-19 once they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

In closing, consider what this PNAS news feature states about the risk of vaccine-induced immune enhancement and dysfunction, peculiarly for the elderly, the very people who would demand the protection a vaccine might offer the about:21

"Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) take shown a paradoxical phenomenon:
Some animals or people who received the vaccine and were later exposed to the virus developed more severe 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 immune backfiring, or so-chosen allowed enhancement, may manifest in unlike ways such as antibody-dependent enhancement (ADE), a procedure in which a virus leverages antibodies to help infection; or jail cell-based enhancement, a category that includes allergic inflammation acquired past Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers fence that although ADE has received the nigh attending to date, it is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known near the epidemiology of the virus and its beliefs in the homo trunk.
'There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and good in coronaviruses ... at the University of Northward 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 form allowed complexes, activating the complement system and potentially damaging the airways."


Sources and References

  • 1 International Journal of Clinical Exercise, October 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org Apr xiv, 2020 117 (xv) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • 4 Science Direct Neutralizing Antibody
  • 5 Science Straight Binding Antibody
  • six Twitter, The Immunologist Apr nine, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • eight, nine Swiss Medical Weekly April 16, 2020; 150:w20249
  • 10 Biochemical and Biophysical Research Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE April 2012; 7(iv): e35421 (PDF)
  • thirteen PLOS ONE Apr 2012; seven(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:ten.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, xx Register of Internal Medicine September two, 2020 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the rising of medical technocracy, Lee Merritt, Md, aprox 8 minutes in (Lie No. 1: Decease Risk)
  • xix Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125