Covid Vaccine

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According to a report that examined how informed consent is given to COVID-19 vaccine trial participants, disclosure forms neglect to inform volunteers that the vaccine might make them susceptible to more severe disease if they're exposed to the virus.

The study,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Disease," published in the International Periodical of Clinical Exercise, October 28, 2020, points out that "COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated."

"Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the development and testing of these vaccines suggest 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-xix disease via antibody-dependent enhancement (ADE)," the paper states.
"This chance 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-19 take chances of ADE should have been and should be prominently and independently disclosed to enquiry subjects currently in vaccine trials, also every bit those existence recruited for the trials and futurity patients after vaccine blessing, in gild to run across the medical ethics 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 astringent acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — take revealed a serious concern: The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that mean? In a nutshell, it means that rather than heighten your amnesty confronting the infection, the vaccine really enhances the virus' ability to enter and infect your cells, resulting in more severe disease than had y'all non been vaccinated. 2

This is the exact contrary of what a vaccine is supposed to exercise, and a meaning problem that has been pointed out from the very kickoff of this push for a COVID-xix vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Illness" explains it this style:three

"In full general, virus-specific antibodies are considered antiviral and play an important office in the control of virus infections in a number of ways. Still, in some instances, the presence of specific antibodies tin can be beneficial to the virus. This activeness 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 veterinary importance. These viruses share some mutual features such as preferential replication in macrophages, ability to institute persistence, and antigenic diversity. For some viruses, ADE of infection has go a nifty concern to disease control by vaccination."


Previous Coronavirus Vaccine Efforts Take 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 iii 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 so 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, one time they were challenged with the wild virus, they all became severely ill and died.

The same thing happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory illness that is very similar to that caused past coronaviruses. At that time, they had decided to skip beast trials and go direct to human trials.

"They tested it on I call back about 35 children, and the same affair happened," Kennedy said. "The children developed a champion antibody response — robust, durable. It looked perfect [just when] the children were exposed to the wild virus, they all became sick. 2 of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH."


Neutralizing Versus Binding Antibodies

Coronaviruses produce not simply ane merely two unlike types of antibodies:

  • Neutralizing antibodies,4 also referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodies5 (also known equally not-neutralizing antibodies) that cannot prevent viral infection

Instead of preventing viral infection, binding antibodies trigger an aberrant allowed response known equally "paradoxical immune enhancement." Another way to await at this is your immune system is actually backfiring and non functioning to protect you only really making y'all 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 fasten protein, which is what attaches to the ACE2 receptor of the cell, is the first phase of the two-stage process viruses use to gain entry into cells.

The idea is that past creating the SARS-CoV-2 spike protein, your immune organization volition commence production of antibodies, without making you sick in the process. The key question is, which of the ii types of antibodies are being produced through this process?


Without Neutralizing Antibodies, Wait More Astringent Illness

In an April 2020 Twitter thread,vi The Immunologist noted: "While developing vaccines ... and considering immunity passports, we must first understand the circuitous part of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that have raised concerns well-nigh 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 subject area against reinfection, as is typically the case with many viral illnesses. (Meaning, once you recover from a viral infection, say measles, you're immune and won't contract the illness once more.)

To determine how MERS affects the immune system, 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. As a result, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill over 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 being infected a third time. According to the authors:

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

In other words, if the vaccine does non effect in a robust response in neutralizing antibodies, you might be at risk for more severe lung disease if you're infected with the virus.

And here'southward an of import point: COVID-19 vaccines are Not designed to forestall 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 also known to crusade ADE. As explained in a Swiss Medical Weekly paper published in April 2020:8

"The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and allowed-mediated mechanisms. An additional machinery facilitating viral jail cell entry and subsequent impairment may involve the so-chosen antibody-dependent enhancement (ADE).
ADE is a very well-known cascade of events whereby viruses may infect susceptible cells via interaction between virions complexed with antibodies or complement components and, respectively, Fc or complement receptors, leading to the amplification of their replication.
This miracle is of enormous relevance not only for the agreement of viral pathogenesis, only besides for developing antiviral strategies, notably vaccines ...
At that place are four serotypes of Dengue virus, all eliciting protective amnesty. However, although homotypic protection is long-lasting, cantankerous-neutralizing antibodies against different serotypes are short-lived and may final only up to 2 years.
In Dengue fever, reinfection with a different serotype runs a more severe class when the protective antibody titer wanes. Here, not-neutralizing antibodies take over neutralizing ones, bind to Dengue virions, and these complexes mediate the infection of phagocytic cells via interaction with the Fc receptor, in a typical ADE.
In other words, heterotypic antibodies at subneutralizing titres account for ADE in persons infected with a serotype of Dengue virus that is different from the starting time 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 main infection, the longer the filibuster to symptomatic secondary infection ..."

The paper goes on to detail results from follow-upwardly investigations into the Dengue vaccine, which revealed the hospitalization charge per unit for Dengue amidst vaccinated children under the age of 9 was greater than the rate among controls. The explanation for this appears to exist that the vaccine mimicked a chief infection, and as that immunity waned, the children became susceptible to ADE when they encountered the virus a second fourth dimension. The author explains:

"A mail hoc analysis of efficacy trials, using an anti-nonstructural protein 1 immunoglobulin G (IgG) enzyme-linked immunosorbent analysis (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 take a chance of severe clinical outcome was increased among seronegative persons.
Based on this, a Strategic Advisor Grouping of Experts convened by World Health 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 finish upwards being important for the COVID-nineteen vaccine. Hypothetically speaking, if SARS-CoV-ii works similar Dengue, which is too caused by an RNA virus, then anyone who has non tested positive for SARS-CoV-2 might really be at increased run a risk for severe COVID-19 after vaccination, and simply those who have already recovered from a bout of COVID-19 would exist protected against severe illness past the vaccine.

To exist clear, nosotros practice not know whether that is the case or not, but these are important areas of inquiry and the current vaccine trials volition merely not be able to answer this important question.

The Swiss Medical Weekly paper 9 also reviews the evidence of ADE in coronavirus infections, citing inquiry 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 diverseness of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The paper too cites research showing "Antibodies elicited by a SARS-CoV vaccine enhanced infection of B prison cell lines in spite of protective responses in the hamster model." Another paper,10 "Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Fasten 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 by diluted antibodies confronting envelope spike proteins rather than nucleocapsid proteins. We 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 against SARS-CoV spike proteins may trigger ADE furnishings. The data heighten new questions regarding a potential SARS-CoV vaccine ..."

A written reportxi 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 ended upward 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 acute 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 Claiming with the SARS Virus," demonstrates what many researchers now fright, namely that COVID-19 vaccines may end up 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 once challenged with the SARS virus. Every bit noted by the authors: thirteen

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 establish the same immunopathologic reaction in animals given South protein vaccine but, although information technology appeared to be of lesser intensity.

Thus, a Th2-type immunopathologic reaction on claiming of vaccinated animals has occurred in three of four animal models (not in hamsters) including two unlike inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine training that does not induce this effect in mice, ferrets and nonhuman primates has non been reported.

This combined experience provides business organisation 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 'condom.' However, the show for safety is for a short catamenia of observation.

The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the ground for developing a vaccine for SARS. Additional safety concerns relate to effectiveness and safety against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, particularly those of the blazon 2 group."


The Elderly Are Near 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 also the most vulnerable to ADE. Preliminary research findingsxiv posted on the preprint server medRxiv at the cease of March 2020 reported that eye-aged and elderly COVID-xix patients accept far higher levels of anti-spike antibodies — which, over again, increase infectivity — than younger patients.


Allowed Enhancement Is a Serious Concern

Some other paper worth mentioning is the May 2020 mini reviewfifteen "Impact of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Evolution." Equally 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 organisation. Experimental studies have suggested the possibility of immune-enhanced illness of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-ii infection ...
Allowed enhancement of illness can theoretically occur in ii ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-ii infection into target cells.
Secondly, antibodies could raise inflammation and hence severity of pulmonary disease. An overview of these antibiotic dependent infection and immunopathology enhancement furnishings are summarized in Fig. ane ...
Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early on phase clinical trials. Animal studies on these CoVs have shown that the spike (Due south) protein-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective against wild-type CoV challenge.
Vaccines that target other parts of the virus, such equally the nucleocapsid, without the Due south poly peptide, have shown no protection against CoV infection and increased lung pathology. Nonetheless, immunization with some Due south protein based CoV vaccines have besides displayed signs of enhanced lung pathology following claiming.
Hence, besides the option of antigen target, vaccine efficacy and hazard of immunopathology may exist dependent on other ancillary factors, including adjuvant formulation, age at vaccination ... and road of immunization."

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

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


Practice a Risk-Do good Assay Earlier Making Up Your Mind

In all likelihood, regardless of how constructive (or ineffective) the COVID-19 vaccines terminate up being, they'll be released to the public in relatively brusque guild. Most predict 1 or more than vaccines will be ready sometime in 2021.

Ironically, the data 17,18,19 we at present 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 lx. xx If you lot're nether the age of forty, your adventure of dying from COVID-19 is merely 0.01%, meaning you have a 99.99% adventure 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 against with a COVID-19 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 in one case you're exposed to the virus. That seems like a lot of take chances for a truly questionable benefit.

To circle back 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 than astringent COVID-19 once they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

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

"Since the 1960s, tests of vaccine candidates for diseases such equally 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 later exposed to the virus developed more than severe illness 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 process in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation acquired by Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers debate that although ADE has received the most attention to appointment, information technology is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its beliefs in the human being body.
'In that location is the potential for ADE, only 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, anile 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 course immune complexes, activating the complement arrangement and potentially damaging the airways."


Sources and References

  • 1 International Journal of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
  • ii, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • 4 Science Direct Neutralizing Antibiotic
  • 5 Science Directly Binding Antibiotic
  • 6 Twitter, The Immunologist April 9, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • 8, nine Swiss Medical Weekly April 16, 2020; 150:w20249
  • 10 Biochemical and Biophysical Research Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE April 2012; 7(4): e35421 (PDF)
  • 13 PLOS ONE Apr 2012; seven(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:10.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • xvi EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September 2, 2020 DOI: x.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the ascent of medical technocracy, Lee Merritt, MD, aprox 8 minutes in (Lie No. i: Decease Risk)
  • 19 Technical Report June 2020 DOI: 10.13140/RG.ii.24350.77125