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 brand them susceptible to more severe illness if they're exposed to the virus.

The study,ane "Informed Consent Disclosure to Vaccine Trial Subjects of Hazard of COVID-19 Vaccine Worsening Clinical Disease," published in the International Journal of Clinical Practice, Oct 28, 2020, points out that "COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe affliction than if they were not vaccinated."

"Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the development 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 fasten to arm-twist neutralizing antibodies), be they composed of protein, viral vector, Deoxyribonucleic acid or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE)," the paper states.
"This run a 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-xix take chances of ADE should have been and should be prominently and independently disclosed to enquiry subjects currently in vaccine trials, also as those being recruited for the trials and future patients later on vaccine blessing, in order to meet the medical ethics standard of patient comprehension for informed consent."


What Is Antibody-Dependent Enhancement?

Equally noted by the authors of that International Periodical of Clinical Exercise paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Center East 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 against the infection, the vaccine actually enhances the virus' ability to enter and infect your cells, resulting in more severe disease than had y'all not been vaccinated. 2

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 get-go of this button for a COVID-19 vaccine. The 2003 review newspaper "Antibody-Dependent Enhancement of Virus Infection and Disease" explains it this way:3

"In general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. Still, in some instances, the presence of specific antibodies tin be beneficial to the virus. This activity is known every bit antibody-dependent enhancement (ADE) of virus infection.
The ADE of virus infection is a phenomenon in which virus-specific antibodies raise 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, ability to found persistence, and antigenic multifariousness. For some viruses, ADE of infection has become a peachy 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 thirty promising candidates.

Of those, the 4 best vaccine candidates were then 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 next. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, once they were challenged with the wild virus, they all became severely ill and died.

The same matter 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 time, they had decided to skip animal trials and go direct to man trials.

"They tested it on I recall about 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 sick. Two of them died. They abased the vaccine. Information technology was a big embarrassment to FDA and NIH."


Neutralizing Versus Binding Antibodies

Coronaviruses produce non only 1 just two different types of antibodies:

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

Instead of preventing viral infection, binding antibodies trigger an abnormal allowed response known equally "paradoxical immune enhancement." Another manner to wait at this is your allowed arrangement is really backfiring and not functioning to protect you lot just actually making you worse.

Many of the COVID-nineteen vaccines currently in the running are using mRNA to instruct your cells to make the SARS-CoV-2 fasten poly peptide (S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the get-go stage of the two-stage process viruses employ to gain entry into cells.

The idea is that by creating the SARS-CoV-ii spike protein, your allowed system volition embark product of antibodies, without making yous sick in the process. The key question is, which of the ii types of antibodies are being produced through this process?


Without Neutralizing Antibodies, Expect More than Astringent Illness

In an April 2020 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering amnesty passports, nosotros must first understand the complex role of antibodies in SARS, MERS and COVID-19." He goes on to listing 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 Antibiotic," which investigated whether getting infected with MERS would protect the field of study confronting reinfection, every bit is typically the case with many viral illnesses. (Meaning, once y'all recover from a viral infection, say measles, you're immune and won't contract the illness once again.)

To determine how MERS affects the allowed organization, the researchers infected white rabbits with the virus. The rabbits got sick and adult antibodies, just those antibodies were not the neutralizing kind, meaning the kind of antibodies that block infection. As a consequence, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill once again, and more severely and 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 tertiary 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 antibody response, or persons whose neutralizing antibody titers take waned, may be at risk for astringent lung illness on re-exposure to MERS-CoV."

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

And here's an of import indicate: COVID-19 vaccines are NOT designed to forbid 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. As explained in a Swiss Medical Weekly paper published in April 2020:eight

"The pathogenesis of COVID-19 is currently believed to proceed via both straight cytotoxic and immune-mediated mechanisms. An additional machinery facilitating viral cell entry and subsequent impairment may involve the and then-chosen antibiotic-dependent enhancement (ADE).
ADE is a very well-known cascade of events whereby viruses may infect susceptible cells via interaction betwixt virions complexed with antibodies or complement components and, respectively, Fc or complement receptors, leading to the amplification of their replication.
This phenomenon is of enormous relevance not only for the understanding of viral pathogenesis, simply also for developing antiviral strategies, notably vaccines ...
At that place are four serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies confronting different serotypes are short-lived and may last just upward to 2 years.
In Dengue fever, reinfection with a different serotype runs a more severe course when the protective antibody titer wanes. Hither, non-neutralizing antibodies take over neutralizing ones, demark to Dengue virions, and these complexes mediate the infection of phagocytic cells via interaction with the Fc receptor, in a typical ADE.
In other words, heterotypic antibodies at subneutralizing titres account for ADE in persons infected with a serotype of Dengue virus that is dissimilar from the first infection.
Cantankerous-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the master 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 amongst 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 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 one 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 against severe Dengue [in] those who had been exposed to the natural infection before vaccination, and that the risk of severe clinical effect was increased among seronegative persons.
Based on this, a Strategic Advisor Grouping of Experts convened by World Wellness Organization (WHO) concluded that only Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could end up being of import for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, and then anyone who has not tested positive for SARS-CoV-2 might actually exist at increased risk for severe COVID-19 afterwards 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 do not know whether that is the instance or not, but these are important areas of enquiry and the current vaccine trials volition simply not be 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 aforementioned FIPV serotype as that in the vaccine.

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

The newspaper likewise 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,10 "Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins," published in 2014, found 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 betoken that SARS-CoV ADE is primarily mediated by 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 suggest that antibodies confronting SARS-CoV spike proteins may trigger ADE effects. The data heighten 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 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 Claiming With SARS-CoV

An interesting 2012 newspaper 12 with the telling title, "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Claiming with the SARS Virus," demonstrates what many researchers now fear, namely that COVID-19 vaccines may end upwards making people more than decumbent to astringent SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunopathology once 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 subsequently challenge.

As indicated, two reports attributed the immunopathology to presence of the Due north protein in the vaccine; however, we plant the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to exist of bottom intensity.

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four animal models (not in hamsters) including 2 different inbred mouse strains with iv different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine preparation 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 accept been conducted and reported to induce antibody responses and to be 'safety.' Nevertheless, the evidence for safe is for a short period of observation.

The business arising from the present study is for an immunopathologic reaction occurring amid 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 safety of vaccinated persons exposed to other coronaviruses, particularly those of the type ii group."


The Elderly Are Most Vulnerable to ADE

On pinnacle of all of these concerns, there'southward prove showing the elderly — who are most vulnerable to severe COVID-19 — are also the virtually vulnerable to ADE. Preliminary research findingsxiv posted on the preprint server medRxiv at the terminate of March 2020 reported that eye-aged and elderly COVID-nineteen patients have far college levels of anti-spike antibodies — which, once again, increase infectivity — than younger patients.


Immune Enhancement Is a Serious Business organization

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

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-two are promising, they both pose a common theoretical safety concern. Experimental studies have suggested the possibility of allowed-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection ...
Allowed enhancement of disease tin 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 illness. An overview of these antibiotic dependent infection and immunopathology enhancement effects are summarized in Fig. i ...
Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Brute studies on these CoVs have shown that the spike (S) protein-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective confronting wild-type CoV challenge.
Vaccines that target other parts of the virus, such every bit the nucleocapsid, without the S protein, have shown no protection against CoV infection and increased lung pathology. Yet, immunization with some Due south protein based CoV vaccines have too displayed signs of enhanced lung pathology post-obit challenge.
Hence, also the choice of antigen target, vaccine efficacy and chance of immunopathology may be dependent on other coincident factors, including adjuvant formulation, 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 circuitous internalization is mediated past the appointment of activating Fc receptors on the cell surface. Co-ligation of inhibitory receptors and so results in the inhibition of antiviral responses which leads to increased viral replication. Right panel: 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 affliction pathology.


Do a Risk-Benefit Analysis Earlier Making Up Your Mind

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

Ironically, the data 17,18,19 we now have no longer support a mass vaccination mandate, because the lethality of COVID-19 is lower than the flu for those under the age of sixty. twenty If you're nether the age of 40, your take chances of dying from COVID-19 is merely 0.01%, meaning you lot accept a 99.99% hazard of surviving the infection. And you could improve that to 99.999% if you're metabolically flexible and vitamin D replete.

Then, really, what are we protecting confronting with a COVID-nineteen vaccine? As mentioned, the vaccines aren't even designed to forbid infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you're exposed to the virus. That seems like a lot of risk for a truly questionable do good.

To circumvolve back to where we started, participants in current COVID-19 vaccine trials are not beingness told of this risk — that by getting the vaccine they may terminate up with more severe COVID-19 once they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

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

"Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and astringent acute 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 severe illness than those who had not been vaccinated. The vaccine-primed allowed system, in certain cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or and then-called immune enhancement, may manifest in unlike ways such as antibody-dependent enhancement (ADE), a procedure in which a virus leverages antibodies to assistance 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 argue that although ADE has received the most attention to date, it is less likely than the other allowed enhancement pathways to crusade a dysregulated response to COVID-nineteen, given what is known almost the epidemiology of the virus and its behavior in the human being torso.
'In that location is the potential for ADE, simply the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the University of Due north Carolina at Chapel Hill.
In previous studies of SARS, aged mice were constitute 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 dissentious the airways."


Sources and References

  • 1 International Journal of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
  • two, 21 PNAS.org April xiv, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;sixteen(1):69-86
  • 4 Science Straight Neutralizing Antibody
  • 5 Science Direct Binding Antibody
  • 6 Twitter, The Immunologist April 9, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • 8, 9 Swiss Medical Weekly April 16, 2020; 150:w20249
  • ten Biochemical and Biophysical Research Communications Baronial 22, 2014; 451(2): 208-214
  • eleven JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS I Apr 2012; 7(four): e35421 (PDF)
  • 13 PLOS ONE April 2012; 7(4): e35421 (PDF), page 11
  • xiv medRxiv DOI:ten.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • xvi EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Register of Internal Medicine September 2, 2020 DOI: x.7326/M20-5352
  • xviii YouTube, SARS-CoV-2 and the ascent of medical technocracy, Lee Merritt, MD, aprox 8 minutes in (Lie No. i: Death Adventure)
  • 19 Technical Written report June 2020 DOI: 10.13140/RG.2.24350.77125