Covid Vaccine

© Paradigm by Gerd Altmann from Pixabay

According to a written report that examined how informed consent is given to COVID-xix vaccine trial participants, disclosure forms neglect to inform volunteers that the vaccine might make them susceptible to more astringent disease if they're exposed to the virus.

The written report,ane "Informed Consent Disclosure to Vaccine Trial Subjects of Take chances of COVID-19 Vaccine Worsening Clinical Disease," published in the International Periodical of Clinical Practice, Oct 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 canonical, and the data generated in the evolution and testing of these vaccines suggest a serious mechanistic business: that vaccines designed empirically using the traditional arroyo (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), be they composed of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease 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 risk is unlikely to occur, obviating truly informed consent by subjects in these trials.
The specific and significant COVID-nineteen risk of ADE should have been and should exist prominently and independently disclosed to research subjects currently in vaccine trials, too as those being recruited for the trials and future patients subsequently vaccine blessing, in club to see the medical ethics standard of patient comprehension for informed consent."


What Is Antibiotic-Dependent Enhancement?

As noted by the authors of that International Periodical of Clinical Practice newspaper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle E respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious business organisation: The vaccines take a tendency to trigger antibiotic-dependent enhancement.

What exactly does that mean? In a nutshell, it means that rather than enhance your immunity confronting 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. 2

This is the exact opposite of what a vaccine is supposed to exercise, and a significant problem that has been pointed out from the very start of this button for a COVID-19 vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Disease" explains information technology this way:3

"In full general, virus-specific antibodies are considered antiviral and play an important role in the command of virus infections in a number of ways. All the same, in some instances, the presence of specific antibodies can exist benign 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 miracle 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, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has go a great business concern to disease control by vaccination."


Previous Coronavirus Vaccine Efforts Accept 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. Past 2012, Chinese, American and European scientists were working on SARS vaccine development, and had near 30 promising candidates.

Of those, the four best vaccine candidates were then given to ferrets, which are the closest counterpart 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, once they were challenged with the wild virus, they all became severely ill and died.

The aforementioned affair happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory disease that is very similar to that caused by coronaviruses. At that fourth dimension, they had decided to skip animal trials and go straight to human trials.

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


Neutralizing Versus Bounden Antibodies

Coronaviruses produce not just ane but two unlike types of antibodies:

  • Neutralizing antibodies,4 likewise referred to as immunoglobulin K (IgG) antibodies, that fight the infection
  • Bounden antibodies5 (also known as non-neutralizing antibodies) that cannot prevent viral infection

Instead of preventing viral infection, bounden antibodies trigger an abnormal immune response known equally "paradoxical immune enhancement." Another manner to wait at this is your allowed system is actually backfiring and not functioning to protect y'all but actually 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-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-phase procedure viruses use to gain entry into cells.

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


Without Neutralizing Antibodies, Expect More than Severe Illness

In an April 2020 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering immunity passports, nosotros must first sympathize the complex function of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that have raised concerns most ADE.

The first is a 2017 written report7 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 field of study confronting reinfection, as is typically the case with many viral illnesses. (Meaning, once y'all recover from a viral infection, say measles, you're allowed and won't contract the illness again.)

To determine how MERS affects the immune organization, 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. Equally a result, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill once 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 2d infection, preventing the animals from existence infected a tertiary time. According to the authors:

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

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

And here'southward an important 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 expiry rates.

ADE in Dengue Infections

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

"The pathogenesis of COVID-19 is currently believed to go on via both directly cytotoxic and allowed-mediated mechanisms. An boosted mechanism facilitating viral cell entry and subsequent damage may involve the so-called antibody-dependent enhancement (ADE).
ADE is a very well-known pour 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 not merely for the understanding of viral pathogenesis, but also for developing antiviral strategies, notably vaccines ...
In that location are four serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against unlike serotypes are curt-lived and may last merely up to 2 years.
In Dengue fever, reinfection with a unlike serotype runs a more than astringent form when the protective antibiotic titer wanes. Hither, 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 different 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 primary infection, the longer the delay to symptomatic secondary infection ..."

The paper goes on to item results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue among vaccinated children under the age of 9 was greater than the rate among controls. The explanation for this appears to be that the vaccine mimicked a primary infection, and equally that immunity waned, the children became susceptible to ADE when they encountered the virus a 2nd time. The author explains:

"A mail hoc assay of efficacy trials, using an anti-nonstructural poly peptide one immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-type 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 run a risk of severe clinical outcome was increased amid seronegative persons.
Based on this, a Strategic Counselor Grouping of Experts convened past Globe Health Organization (WHO) concluded that just Dengue seropositive persons should exist vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could cease up existence important for the COVID-nineteen vaccine. Hypothetically speaking, if SARS-CoV-two works like Dengue, which is as well caused by an RNA virus, and then anyone who has not tested positive for SARS-CoV-2 might actually be at increased take a chance for severe COVID-nineteen afterwards vaccination, and simply those who have already recovered from a bout of COVID-19 would be protected against severe disease by the vaccine.

To be clear, we practise not know whether that is the example or not, but these are important areas of research and the electric current vaccine trials will simply not be able to respond this important question.

The Swiss Medical Weekly newspaper 9 also reviews the prove 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 accept shown immunization with a diversity of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The paper also 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." Some other paper,ten "Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins," published in 2014, institute 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 past diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. Nosotros besides generated monoclonal antibodies against SARS-CoV spike proteins and observed that most of them promoted SARS-CoV infection.

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

A 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 fasten poly peptide concluded 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 astute lengthened alveolar damage, likely 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 fear, namely that COVID-19 vaccines may end up making people more decumbent to severe SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a diverseness 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-blazon immunopathologic in lungs later on claiming.

Every bit indicated, 2 reports attributed the immunopathology to presence of the N protein in the vaccine; yet, nosotros institute the same immunopathologic reaction in animals given S poly peptide vaccine but, although information technology appeared to be of lesser intensity.

Thus, a Th2-blazon immunopathologic reaction on claiming of vaccinated animals has occurred in three of four beast models (not in hamsters) including two dissimilar inbred mouse strains with 4 different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine preparation that does not induce this upshot 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 exist 'safe.' However, the prove for safety is for a short period of observation.

The concern arising from the present report is for an immunopathologic reaction occurring amid vaccinated individuals on exposure to infectious SARS-CoV, the basis 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 blazon ii group."


The Elderly Are Almost Vulnerable to ADE

On peak of all of these concerns, in that location'southward evidence showing the elderly — who are nigh vulnerable to severe COVID-19 — are also the nearly 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 take far higher levels of anti-fasten antibodies — which, again, increment infectivity — than younger patients.


Immune Enhancement Is a Serious Concern

Another paper worth mentioning is the May 2020 mini reviewxv "Impact of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development." As in many other papers, the authors point out that:16

"While evolution of both hyperimmune globulin therapy and vaccine confronting SARS-CoV-two are promising, they both pose a common theoretical safe concern. Experimental studies have suggested the possibility of immune-enhanced affliction of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-ii infection ...
Immune enhancement of disease can theoretically occur in two 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 antibiotic dependent infection and immunopathology enhancement effects are summarized in Fig. i ...
Currently, at that place 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 (Southward) poly peptide-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, take shown no protection against CoV infection and increased lung pathology. Nevertheless, immunization with some S poly peptide based CoV vaccines have as well displayed signs of enhanced lung pathology following challenge.
Hence, besides the choice of antigen target, vaccine efficacy and risk of immunopathology may be dependent on other ancillary factors, including adjuvant conception, age at vaccination ... and route of immunization."

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

© articles.mercola.com
Figure 1: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex internalization is mediated by the date of activating Fc receptors on the cell surface. Co-ligation of inhibitory receptors then results in the inhibition of antiviral responses which leads to increased viral replication. Right console: Antibodies can crusade immunopathology by activating the complement pathway or antibiotic-dependent cellular cytotoxicity (ADCC). For both pathways, excessive immune activation results in the release of cytokines and chemokines, leading to enhanced affliction pathology.


Do a Risk-Benefit Assay Before Making Up Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end up beingness, they'll be released to the public in relatively short order. Well-nigh predict one or more vaccines will exist ready sometime in 2021.

Ironically, the information 17,18,19 we at present accept no longer back up a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60. 20 If you're under the historic period of twoscore, your risk of dying from COVID-nineteen 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.

And so, actually, what are nosotros protecting against with a COVID-19 vaccine? Equally mentioned, the vaccines aren't fifty-fifty designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially make y'all sicker once y'all're exposed to the virus. That seems like a lot of risk for a truly questionable benefit.

To circle dorsum to where we started, participants in current COVID-19 vaccine trials are not being told of this risk — that by getting the vaccine they may end up with more severe COVID-19 in one case they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

In closing, consider what this PNAS news feature states well-nigh the adventure of vaccine-induced immune enhancement and dysfunction, especially 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 not been vaccinated. The vaccine-primed immune system, in sure cases, seemed to launch a shoddy response to the natural infection ...
This allowed backfiring, or so-chosen immune enhancement, may manifest in different ways such equally antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers debate that although ADE has received the most attention to date, information technology is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-nineteen, given what is known about the epidemiology of the virus and its beliefs in the man body.
'There is the potential for ADE, only the bigger trouble is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the Academy of Northward Carolina at Chapel Hill.
In previous studies of SARS, aged mice were found to have particularly high risks of life-threatening Th2 immunopathology ... in which a faulty T prison 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

  • one International Journal of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
  • ii, 21 PNAS.org April xiv, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • 4 Scientific discipline Direct Neutralizing Antibody
  • 5 Science Straight Binding Antibody
  • vi Twitter, The Immunologist Apr 9, 2020
  • 7 PLOS Pathogens 2017 Aug; xiii(8): e1006565
  • viii, 9 Swiss Medical Weekly Apr 16, 2020; 150:w20249
  • 10 Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE Apr 2012; 7(4): e35421 (PDF)
  • 13 PLOS I April 2012; 7(4): e35421 (PDF), folio xi
  • 14 medRxiv DOI:x.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • sixteen EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, xx Annals of Internal Medicine September ii, 2020 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, Medico, aprox 8 minutes in (Lie No. i: Death Chance)
  • xix Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125