Covid Vaccine

© Paradigm past Gerd Altmann from Pixabay

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

The study,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Run a risk of COVID-19 Vaccine Worsening Clinical Disease," published in the International Journal 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 non 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 organization: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral fasten to elicit neutralizing antibodies), be they equanimous 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 risk is unlikely to occur, obviating truly informed consent past subjects in these trials.
The specific and significant COVID-nineteen gamble 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 time to come patients after vaccine approval, in order to meet the medical ethics standard of patient comprehension for informed consent."


What Is Antibiotic-Dependent Enhancement?

Every bit noted by the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle Eastward respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious business: The vaccines have a tendency to trigger antibody-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' ability to enter and infect your cells, resulting in more severe affliction than had yous not been vaccinated. 2

This is the exact opposite of what a vaccine is supposed to do, and a meaning trouble that has been pointed out from the very beginning of this push for a COVID-19 vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Affliction" explains it this way:iii

"In general, virus-specific antibodies are considered antiviral and play an important office in the command of virus infections in a number of ways. All the same, in some instances, the presence of specific antibodies tin be beneficial to the virus. This activity 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 wellness and veterinarian importance. These viruses share some common features such as preferential replication in macrophages, ability to found persistence, and antigenic diversity. For some viruses, ADE of infection has become a great 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, post-obit three consecutive SARS outbreaks. Past 2012, Chinese, American and European scientists were working on SARS vaccine development, and had about 30 promising candidates.

Of those, the iv 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 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 affair happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory illness that is very similar to that caused by coronaviruses. At that time, they had decided to skip animate being trials and become directly to human trials.

"They tested it on I think about 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 ill. Two of them died. They abased the vaccine. It was a big embarrassment to FDA and NIH."


Neutralizing Versus Bounden Antibodies

Coronaviruses produce not just one simply two different types of antibodies:

  • Neutralizing antibodies,iv also referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodiesfive (too known every bit non-neutralizing antibodies) that cannot prevent viral infection

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known every bit "paradoxical immune enhancement." Another way to look at this is your allowed system is really backfiring and not functioning to protect y'all 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-2 spike poly peptide (S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the first stage of the two-stage process viruses employ to proceeds entry into cells.

The idea is that past creating the SARS-CoV-two fasten protein, your immune system volition commence product of antibodies, without making y'all sick in the process. The cardinal question is, which of the two types of antibodies are beingness produced through this process?


Without Neutralizing Antibodies, Expect More Severe Illness

In an Apr 2020 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering immunity 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 have raised concerns virtually ADE.

The first is a 2017 report7 in PLOS Pathogens, "Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absence of Neutralizing Antibiotic," which investigated whether getting infected with MERS would protect the subject area against reinfection, as is typically the case with many viral illnesses. (Meaning, once yous recover from a viral infection, say measles, you're immune and won't contract the illness again.)

To determine how MERS affects the immune system, the researchers infected white rabbits with the virus. The rabbits got sick and developed antibodies, simply those antibodies were not the neutralizing kind, significant the kind of antibodies that block infection. As a result, they were non protected from reinfection, and when exposed to MERS for a second time, they became ill again, and more than 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 being infected a 3rd 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 antibody titers have waned, may be at risk for severe lung disease 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 risk for more astringent lung disease if yous're infected with the virus.

And hither's an of import betoken: COVID-19 vaccines are Non designed to prevent infection. As detailed in "How COVID-19 Vaccine Trials Are Rigged," a "successful" vaccine simply needs to reduce the severity of the symptoms. They're non even looking at reducing infection, hospitalization or death rates.

ADE in Dengue Infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly newspaper published in April 2020:8

"The pathogenesis of COVID-nineteen is currently believed to go on 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 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 simply for the agreement of viral pathogenesis, but also for developing antiviral strategies, notably vaccines ...
At that place are 4 serotypes of Dengue virus, all eliciting protective amnesty. However, although homotypic protection is long-lasting, cantankerous-neutralizing antibodies against dissimilar serotypes are short-lived and may last only upward to 2 years.
In Dengue fever, reinfection with a different serotype runs a more astringent course when the protective antibody titer wanes. Here, not-neutralizing antibodies accept 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 post-obit the primary infection, the longer the delay to symptomatic secondary infection ..."

The paper goes on to detail results from follow-upwardly 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 second fourth dimension. The author explains:

"A post hoc analysis of efficacy trials, using an anti-nonstructural protein one 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 severe Dengue [in] those who had been exposed to the natural infection before vaccination, and that the hazard of severe clinical upshot was increased amidst seronegative persons.
Based on this, a Strategic Counselor Group of Experts convened by World Wellness Arrangement (WHO) concluded that simply 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 also caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually exist at increased take a chance for severe COVID-19 after vaccination, and only those who have already recovered from a bout of COVID-19 would be protected against severe disease by the vaccine.

To be clear, we exercise non know whether that is the instance or not, simply these are of import areas of inquiry and the current vaccine trials will simply not be able to respond this important question.

The Swiss Medical Weekly paper ix besides reviews the bear witness 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 aforementioned FIPV serotype as that in the vaccine.

Experiments have shown immunization with a variety of SARS vaccines resulted in pulmonary immunopathology one time challenged with the SARS virus.

The paper also 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 paper,x "Antibody-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 college levels of apoptosis.

Results from infectivity assays indicate that SARS-CoV ADE is primarily mediated past diluted antibodies against envelope fasten 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 suggest that antibodies confronting SARS-CoV spike proteins may trigger ADE effects. The data raise 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 protein concluded upward 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 acute diffuse alveolar damage, likely past "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Later on 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 end upwardly making people more prone to severe SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunopathology in one case challenged with the SARS virus. Every bit noted past 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-type immunopathologic in lungs after challenge.

As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; yet, we found the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to exist of lesser intensity.

Thus, a Th2-type immunopathologic reaction on claiming of vaccinated animals has occurred in three of iv animal models (not in hamsters) including two different inbred mouse strains with 4 different 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 non been reported.

This combined experience provides business organization 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 'rubber.' However, the testify for safety is for a brusk flow of ascertainment.

The concern arising from the present study is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the footing for developing a vaccine for SARS. Boosted condom concerns chronicle to effectiveness and safety against antigenic variants of SARS-CoV and for prophylactic of vaccinated persons exposed to other coronaviruses, particularly those of the type ii grouping."


The Elderly Are Most Vulnerable to ADE

On top of all of these concerns, there's evidence showing the elderly — who are most vulnerable to astringent COVID-19 — are likewise the nearly vulnerable to ADE. Preliminary research findingsxiv posted on the preprint server medRxiv at the end of March 2020 reported that centre-aged and elderly COVID-19 patients have far higher levels of anti-fasten antibodies — which, once more, increase infectivity — than younger patients.


Immune Enhancement Is a Serious Business organisation

Another paper worth mentioning is the May 2020 mini review15 "Bear on of Immune Enhancement on COVID-xix Polyclonal Hyperimmune Globulin Therapy and Vaccine Development." As in many other papers, the authors point out that:16

"While development of both hyperimmune globulin therapy and vaccine confronting SARS-CoV-2 are promising, they both pose a common theoretical safety concern. Experimental studies accept suggested the possibility of immune-enhanced affliction of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection ...
Allowed enhancement of disease can theoretically occur in 2 ways. Firstly, not-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 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 stage clinical trials. Animal studies on these CoVs accept shown that the spike (S) 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 protein, accept shown no protection against CoV infection and increased lung pathology. However, immunization with some Due south protein based CoV vaccines take also 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, historic period at vaccination ... and route of immunization."

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

© manufactures.mercola.com
Figure ane: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex internalization is mediated past the engagement of activating Fc receptors on the prison cell surface. Co-ligation of inhibitory receptors and then results in the inhibition of antiviral responses which leads to increased viral replication. Correct console: Antibodies can cause immunopathology by 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 disease pathology.


Practise a Take a chance-Do good Analysis Before Making Up Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines cease upwardly being, they'll be released to the public in relatively short order. Near predict one or more vaccines will be gear up quondam in 2021.

Ironically, the data 17,18,nineteen nosotros at present have no longer support a mass vaccination mandate, considering the lethality of COVID-nineteen is lower than the flu for those under the historic period of 60. twenty If y'all're under the age of 40, your take a chance of dying from COVID-19 is just 0.01%, pregnant you have a 99.99% risk of surviving the infection. And y'all could ameliorate that to 99.999% if y'all're metabolically flexible and vitamin D replete.

So, really, what are nosotros protecting confronting with a COVID-nineteen vaccine? As 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 in one case you're exposed to the virus. That seems like a lot of run a risk for a truly questionable benefit.

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


Lethal Th2 Immunopathology Is Some other Potential Hazard

In endmost, consider what this PNAS news feature states about the risk 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 every bit dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) accept 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 organisation, in certain cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or so-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 caused by Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers debate that although ADE has received the most attending 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 nigh the epidemiology of the virus and its behavior in the human being trunk.
'There is the potential for ADE, just the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the Academy of North Carolina at Chapel Loma.
In previous studies of SARS, aged 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: 10.111/ijcp.13795
  • two, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;sixteen(1):69-86
  • 4 Science Straight Neutralizing Antibody
  • v Science Directly Binding Antibody
  • 6 Twitter, The Immunologist April 9, 2020
  • vii PLOS Pathogens 2017 Aug; xiii(8): e1006565
  • viii, 9 Swiss Medical Weekly April 16, 2020; 150:w20249
  • 10 Biochemical and Biophysical Research Communications August 22, 2014; 451(2): 208-214
  • xi JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE April 2012; seven(four): e35421 (PDF)
  • 13 PLOS Ane April 2012; vii(4): e35421 (PDF), folio 11
  • 14 medRxiv DOI:10.1101/2020.03.thirty.20047365 (PDF)
  • fifteen EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, xx Annals of Internal Medicine September 2, 2020 DOI: x.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the rising of medical technocracy, Lee Merritt, MD, aprox viii minutes in (Lie No. i: Decease Take chances)
  • 19 Technical Written report June 2020 DOI: 10.13140/RG.2.24350.77125