Covid Vaccine

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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 report,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Take a chance of COVID-nineteen Vaccine Worsening Clinical Disease," published in the International Journal of Clinical Exercise, Oct 28, 2020, points out that "COVID-nineteen vaccines designed to arm-twist neutralizing antibodies may sensitize vaccine recipients to more than severe disease than if they were non vaccinated."

"Vaccines for SARS, MERS and RSV have never been approved, and the information generated in the evolution 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, Deoxyribonucleic acid or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE)," the paper states.
"This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-xix vaccine trials that acceptable patient comprehension of this gamble is unlikely to occur, obviating truly informed consent by subjects in these trials.
The specific and significant COVID-19 risk of ADE should have been and should be prominently and independently disclosed to inquiry subjects currently in vaccine trials, besides as those being recruited for the trials and time to come patients after vaccine approval, in order to run into the medical ethics standard of patient comprehension for informed consent."


What Is Antibiotic-Dependent Enhancement?

As noted by the authors of that International Periodical of Clinical Practice 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) — accept revealed a serious concern: The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that hateful? In a nutshell, it means that rather than enhance your amnesty against the infection, the vaccine actually enhances the virus' ability to enter and infect your cells, resulting in more severe illness than had you not been vaccinated. two

This is the verbal reverse of what a vaccine is supposed to practice, and a significant problem 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 style:3

"In full general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. Nonetheless, 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 miracle 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 miracle has been reported in vitro and in vivo for viruses representing numerous families and genera of public wellness and veterinary importance. These viruses share some mutual features such as preferential replication in macrophages, ability to found persistence, and antigenic diversity. For some viruses, ADE of infection has become a dandy 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 four best vaccine candidates were then given to ferrets, which are the closest analogue to human lung infections. In the video beneath, which is a select outtake from my total 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 like to that caused by coronaviruses. At that fourth dimension, they had decided to skip fauna trials and go directly to human trials.

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


Neutralizing Versus Binding Antibodies

Coronaviruses produce not just 1 but two dissimilar types of antibodies:

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

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known as "paradoxical immune enhancement." Another way to look at this is your allowed system is really backfiring and not operation to protect you merely actually making yous worse.

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

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


Without Neutralizing Antibodies, Look More Severe Disease

In an April 2020 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering amnesty passports, nosotros must first understand the circuitous role 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 Absence of Neutralizing Antibody," which investigated whether getting infected with MERS would protect the field of study against reinfection, as is typically the case with many viral illnesses. (Meaning, once you lot 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, meaning the kind of antibodies that block infection. As a event, they were not protected from reinfection, and when exposed to MERS for a second time, they became sick again, and more than severely then.

"In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increment in viral RNA titers," the authors noted. Interestingly, neutralizing antibodies were elicited during this second infection, preventing the animals from existence infected a third fourth dimension. Co-ordinate 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 antibody titers accept waned, may be at risk for astringent lung illness on re-exposure to MERS-CoV."

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

And here's an important point: COVID-19 vaccines are Non designed to prevent infection. As detailed in "How COVID-19 Vaccine Trials Are Rigged," a "successful" vaccine merely needs to reduce the severity of the symptoms. They're non fifty-fifty looking at reducing infection, hospitalization or expiry rates.

ADE in Dengue Infections

The Dengue virus is also known to cause 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 straight cytotoxic and allowed-mediated mechanisms. An additional mechanism facilitating viral prison 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 phenomenon is of enormous relevance not but for the understanding of viral pathogenesis, but likewise 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 only upward to ii years.
In Dengue fever, reinfection with a different serotype runs a more astringent grade when the protective antibody titer wanes. Hither, non-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 beginning infection.
Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the college the titer of such antibodies following the principal infection, the longer the delay to symptomatic secondary infection ..."

The paper goes on to particular results from follow-upwardly investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue among vaccinated children under the age of ix was greater than the rate amidst controls. The explanation for this appears to be that the vaccine mimicked a master 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 1 immunoglobulin 1000 (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited past wild-blazon 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 astringent clinical event was increased among seronegative persons.
Based on this, a Strategic Advisor Group of Experts convened by World Health Organization (WHO) ended that but Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could finish upward beingness important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also acquired by an RNA virus, then anyone who has non tested positive for SARS-CoV-two might actually be at increased risk for severe COVID-19 after vaccination, and only those who have already recovered from a bout of COVID-19 would exist protected against severe affliction by the vaccine.

To exist clear, we do non know whether that is the case or non, but these are of import areas of enquiry and the current vaccine trials will only not be able to answer this important question.

The Swiss Medical Weekly paper 9 too 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 variety of SARS vaccines resulted in pulmonary immunopathology once 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 newspaper,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 indicate that SARS-CoV ADE is primarily mediated by diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. Nosotros too generated monoclonal antibodies against SARS-CoV spike proteins and observed that well-nigh of them promoted SARS-CoV infection.

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

A written report11 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-fasten IgG antibodies into unvaccinated macaques, they adult acute diffuse alveolar damage, probable by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection After Challenge With SARS-CoV

An interesting 2012 paper 12 with the telling title, "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus," demonstrates what many researchers now fear, namely that COVID-19 vaccines may end upwardly making people more than prone to severe SARS-CoV-ii infection.

The paper reviews experiments showing immunization with a diverseness of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus. As 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-blazon immunopathologic in lungs later challenge.

Equally indicated, ii reports attributed the immunopathology to presence of the N protein in the vaccine; notwithstanding, we found the aforementioned immunopathologic reaction in animals given S protein vaccine only, although it appeared to exist 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 2 dissimilar inbred mouse strains with 4 dissimilar 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 have been conducted and reported to induce antibody responses and to exist 'safe.' Even so, the testify for rubber is for a short period of observation.

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


The Elderly Are Most Vulnerable to ADE

On top of all of these concerns, at that place'due south evidence showing the elderly — who are almost vulnerable to severe COVID-19 — are also the well-nigh vulnerable to ADE. Preliminary research findingsxiv posted on the preprint server medRxiv at the end of March 2020 reported that middle-aged and elderly COVID-19 patients take far higher levels of anti-spike antibodies — which, again, increment infectivity — than younger patients.


Immune Enhancement Is a Serious Business organisation

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

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical safety business. Experimental studies take suggested the possibility of immune-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection ...
Immune enhancement of disease can theoretically occur in ii means. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can heighten SARS-CoV-2 infection into target cells.
Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. An overview of these antibiotic dependent infection and immunopathology enhancement effects are summarized in Fig. 1 ...
Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animal studies on these CoVs have shown that the spike (S) poly peptide-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 equally the nucleocapsid, without the S protein, take shown no protection confronting CoV infection and increased lung pathology. Even so, immunization with some S protein based CoV vaccines accept likewise displayed signs of enhanced lung pathology following challenge.
Hence, as well the choice of antigen target, vaccine efficacy and take a chance of immunopathology may be dependent on other ancillary factors, including adjuvant formulation, age at vaccination ... and route of immunization."

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

© manufactures.mercola.com
Figure ane: Machinery of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex 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 console: Antibodies can cause immunopathology by activating the complement pathway or antibiotic-dependent cellular cytotoxicity (ADCC). For both pathways, excessive immune activation results in the release of cytokines and chemokines, leading to enhanced disease pathology.


Do a Risk-Benefit Analysis Before Making Upwards Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-xix vaccines terminate upwardly existence, they'll be released to the public in relatively short guild. Almost predict one or more vaccines will exist prepare sometime in 2021.

Ironically, the data 17,eighteen,19 we at present take no longer support a mass vaccination mandate, because the lethality of COVID-19 is lower than the flu for those nether the age of threescore. 20 If y'all're under the age of twoscore, your risk of dying from COVID-19 is just 0.01%, significant you take a 99.99% chance of surviving the infection. And you could improve that to 99.999% if you're metabolically flexible and vitamin D replete.

So, really, what are we protecting against with a COVID-19 vaccine? As mentioned, the vaccines aren't even designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially brand you sicker once you're exposed to the virus. That seems like a lot of risk for a truly questionable benefit.

To circumvolve back to where nosotros started, participants in current COVID-19 vaccine trials are non 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 closing, consider what this PNAS news feature states about the risk of vaccine-induced immune enhancement and dysfunction, peculiarly for the elderly, the very people who would demand the protection a vaccine might offer the most:21

"Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) have shown a paradoxical miracle:
Some animals or people who received the vaccine and were later on exposed to the virus developed more severe disease than those who had non been vaccinated. The vaccine-primed immune 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 different ways such equally antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to assistance infection; or jail 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 attending to date, it is less likely than the other immune enhancement pathways to crusade a dysregulated response to COVID-19, given what is known nearly the epidemiology of the virus and its behavior in the human being body.
'There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and practiced in coronaviruses ... at the University of N Carolina at Chapel Hill.
In previous studies of SARS, aged mice were establish to take specially 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 Periodical of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (fifteen) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • four Science Direct Neutralizing Antibody
  • 5 Science Direct Binding Antibiotic
  • half-dozen Twitter, The Immunologist April 9, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • 8, ix Swiss Medical Weekly April 16, 2020; 150:w20249
  • x Biochemical and Biophysical Research Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: ten.1172/jci.insight.123158
  • 12 PLOS Ane April 2012; vii(four): e35421 (PDF)
  • 13 PLOS ONE April 2012; 7(4): e35421 (PDF), page 11
  • fourteen medRxiv DOI:10.1101/2020.03.xxx.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September two, 2020 DOI: ten.7326/M20-5352
  • eighteen YouTube, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, MD, aprox 8 minutes in (Lie No. 1: Death Risk)
  • 19 Technical Report June 2020 DOI: 10.13140/RG.ii.24350.77125