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 fail to inform volunteers that the vaccine might make them susceptible to more severe illness if they're exposed to the virus.

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

"Vaccines for SARS, MERS and RSV have never been approved, and the information generated in the development and testing of these vaccines advise a serious mechanistic concern: 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 commitment method, may worsen COVID-nineteen disease via antibiotic-dependent enhancement (ADE)," the newspaper 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 by subjects in these trials.
The specific and significant COVID-xix adventure of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well as those beingness recruited for the trials and future patients after vaccine approval, in order to meet the medical ideals standard of patient comprehension for informed consent."


What Is Antibody-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 East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — accept revealed a serious concern: The vaccines accept a trend to trigger antibiotic-dependent enhancement.

What exactly does that mean? In a nutshell, information technology means that rather than enhance your amnesty confronting the infection, the vaccine actually enhances the virus' ability 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 do, and a significant problem that has been pointed out from the very outset of this push button for a COVID-19 vaccine. The 2003 review paper "Antibiotic-Dependent Enhancement of Virus Infection and Disease" explains it this mode:3

"In general, virus-specific antibodies are considered antiviral and play an important function in the control of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This 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 health and veterinarian 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 concern to disease command 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 evolution, which began in 2002, post-obit 3 consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had about 30 promising candidates.

Of those, the four best vaccine candidates were then given to ferrets, which are the closest analogue to human being 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 aforementioned thing 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 animate being trials and get directly to human trials.

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


Neutralizing Versus Binding Antibodies

Coronaviruses produce not just one but 2 dissimilar types of antibodies:

  • Neutralizing antibodies,four also referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodies5 (besides known as non-neutralizing antibodies) that cannot prevent viral infection

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known as "paradoxical immune enhancement." Some other way to await at this is your immune system is actually backfiring and not functioning to protect y'all just really making yous worse.

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

The thought is that by creating the SARS-CoV-2 spike poly peptide, your immune system will embark production of antibodies, without making y'all ill in the process. The key question is, which of the 2 types of antibodies are existence produced through this process?


Without Neutralizing Antibodies, Expect More than Astringent Illness

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

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

To make up one's mind how MERS affects the immune system, the researchers infected white rabbits with the virus. The rabbits got ill and adult antibodies, but those antibodies were non the neutralizing kind, pregnant the kind of antibodies that block infection. Every bit a result, they were non protected from reinfection, and when exposed to MERS for a second time, they became ill again, and more severely so.

"In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers," the authors noted. Interestingly, neutralizing antibodies were elicited during this 2nd infection, preventing the animals from existence infected a third time. 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 have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV."

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

And here'south an important signal: COVID-19 vaccines are Not designed to prevent infection. As detailed in "How COVID-xix 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 also known to cause ADE. As explained in a Swiss Medical Weekly paper published in Apr 2020:8

"The pathogenesis of COVID-nineteen is currently believed to proceed via both directly cytotoxic and allowed-mediated mechanisms. An boosted machinery 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 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 just for the understanding of viral pathogenesis, but as well for developing antiviral strategies, notably vaccines ...
There are four serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may last simply up to ii years.
In Dengue fever, reinfection with a dissimilar serotype runs a more astringent course when the protective antibody titer wanes. Hither, 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 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 filibuster to symptomatic secondary infection ..."

The newspaper goes on to detail results from follow-upward 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 as that immunity waned, the children became susceptible to ADE when they encountered the virus a second time. The writer explains:

"A post hoc assay 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 against astringent 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 Group of Experts convened by World Health System (WHO) concluded that but Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

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

To be clear, we do not know whether that is the instance or not, only these are important areas of inquiry and the current vaccine trials will just non be able to reply this important question.

The Swiss Medical Weekly paper 9 also reviews the evidence 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 have 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 Confronting Spike Proteins," published in 2014, plant 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 fasten proteins rather than nucleocapsid proteins. We also generated monoclonal antibodies against SARS-CoV spike proteins and observed that almost of them promoted SARS-CoV infection.

Combined, our results suggest that antibodies against 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 journal JCI Insight in 2019. Hither, 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 astute diffuse alveolar harm, likely by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Subsequently Claiming With SARS-CoV

An interesting 2012 newspaper 12 with the telling championship, "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 diversity of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus. Equally 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 after challenge.

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

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four animal models (not in hamsters) including two 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 effect 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 have been conducted and reported to induce antibody responses and to be 'safe.' Even so, the evidence for prophylactic is for a brusk period of ascertainment.

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 condom against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, especially those of the type 2 group."


The Elderly Are Most Vulnerable to ADE

On elevation of all of these concerns, there'due south prove showing the elderly — who are most 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, increment infectivity — than younger patients.


Immune Enhancement Is a Serious Concern

Another newspaper worth mentioning is the May 2020 mini review15 "Touch of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Evolution." As in many other papers, the authors point out that:16

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical safe business. Experimental studies take suggested the possibility of allowed-enhanced disease 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 enhance SARS-CoV-two 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. ane ...
Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animal studies on these CoVs accept shown that the spike (S) 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 every bit the nucleocapsid, without the Southward protein, have shown no protection confronting CoV infection and increased lung pathology. However, immunization with some S protein based CoV vaccines have also displayed signs of enhanced lung pathology following challenge.
Hence, likewise the choice of antigen target, vaccine efficacy and risk of immunopathology may exist dependent on other ancillary factors, including adjuvant formulation, historic period at vaccination ... and route of immunization."

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

© manufactures.mercola.com
Figure 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 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 cause immunopathology past 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 disease pathology.


Do a Risk-Benefit Analysis Earlier Making Upwardly Your Listen

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end up being, they'll exist released to the public in relatively short order. Near predict 1 or more vaccines will be ready erstwhile in 2021.

Ironically, the information 17,xviii,xix we now have 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. twenty If you're under the historic period of 40, your risk of dying from COVID-19 is simply 0.01%, meaning y'all have a 99.99% take chances of surviving the infection. And you could amend that to 99.999% if you're metabolically flexible and vitamin D replete.

And so, really, what are we protecting against with a COVID-xix vaccine? As mentioned, the vaccines aren't even designed to prevent infection, simply reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you're exposed to the virus. That seems similar a lot of risk for a truly questionable benefit.

To circle back to where we started, participants in current COVID-nineteen vaccine trials are non 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 about the run a risk of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offering the well-nigh: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 phenomenon:
Some animals or people who received the vaccine and were afterward exposed to the virus adult more severe disease than those who had not been vaccinated. The vaccine-primed allowed system, in sure cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or so-called allowed enhancement, may manifest in different ways such as 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 argue that although ADE has received the nearly attending to appointment, it 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 human body.
'In that location is the potential for ADE, but the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the University of North Carolina at Chapel Hill.
In previous studies of SARS, aged mice were institute to have peculiarly loftier 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 arrangement and potentially dissentious the airways."


Sources and References

  • 1 International Journal of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;16(one):69-86
  • 4 Science Direct Neutralizing Antibody
  • 5 Science Direct Bounden Antibody
  • vi Twitter, The Immunologist April 9, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • 8, 9 Swiss Medical Weekly April 16, 2020; 150:w20249
  • 10 Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: ten.1172/jci.insight.123158
  • 12 PLOS I Apr 2012; vii(4): e35421 (PDF)
  • xiii PLOS Ane April 2012; seven(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:10.1101/2020.03.xxx.20047365 (PDF)
  • fifteen EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Register of Internal Medicine September 2, 2020 DOI: 10.7326/M20-5352
  • eighteen YouTube, SARS-CoV-two and the ascension of medical technocracy, Lee Merritt, MD, aprox 8 minutes in (Lie No. 1: Decease Risk)
  • nineteen Technical Written report June 2020 DOI: 10.13140/RG.2.24350.77125