Covid Vaccine

© Prototype past Gerd Altmann from Pixabay

According to a written report 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 disease if they're exposed to the virus.

The study,ane "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Affliction," published in the International Journal of Clinical Exercise, October 28, 2020, points out that "COVID-nineteen vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe illness 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 propose a serious mechanistic business organisation: that vaccines designed empirically using the traditional approach (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 delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE)," the paper states.
"This take a 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 by subjects in these trials.
The specific and significant COVID-19 take a chance of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, also as those beingness recruited for the trials and future patients after vaccine approval, in order to encounter the medical ideals standard of patient comprehension for informed consent."


What Is Antibiotic-Dependent Enhancement?

As noted by the authors of that International Journal of Clinical Practice newspaper, previous coronavirus vaccine efforts — for astringent acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious concern: The vaccines accept a tendency to trigger antibody-dependent enhancement.

What exactly does that hateful? In a nutshell, it means that rather than enhance your immunity against the infection, the vaccine really enhances the virus' ability to enter and infect your cells, resulting in more severe disease than had you lot not been vaccinated. 2

This is the verbal opposite of what a vaccine is supposed to practise, and a pregnant problem that has been pointed out from the very showtime of this push button for a COVID-19 vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Affliction" 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. However, in some instances, the presence of specific antibodies tin exist beneficial to the virus. This activity is known as antibiotic-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 common features such as preferential replication in macrophages, ability to establish persistence, and antigenic variety. For some viruses, ADE of infection has become a bang-up concern to affliction control by vaccination."


Previous Coronavirus Vaccine Efforts Accept All Failed

In my May 2020 interview above with Robert Kennedy Jr., he summarized the history of coronavirus vaccine evolution, which began in 2002, following 3 consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had nigh thirty promising candidates.

Of those, the four best vaccine candidates were so given to ferrets, which are the closest analogue to man lung infections. In the video below, 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, once they were challenged with the wild virus, they all became severely ill and died.

The same affair happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory affliction that is very similar to that acquired by coronaviruses. At that time, they had decided to skip fauna trials and go directly to human trials.

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


Neutralizing Versus Binding Antibodies

Coronaviruses produce non just ane merely 2 unlike types of antibodies:

  • Neutralizing antibodies,four also referred to as immunoglobulin Thousand (IgG) antibodies, that fight the infection
  • Binding antibodiesfive (as well known as non-neutralizing antibodies) that cannot foreclose viral infection

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

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to brand the SARS-CoV-2 spike protein (S poly peptide). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the first stage of the 2-phase procedure viruses use to gain entry into cells.

The thought is that past creating the SARS-CoV-2 spike protein, your immune organisation will commence production of antibodies, without making you ill 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 Severe Illness

In an April 2020 Twitter thread,vi The Immunologist noted: "While developing vaccines ... and because immunity passports, we must first understand the circuitous role of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that accept raised concerns nigh ADE.

The first is a 2017 studyseven 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 against reinfection, as is typically the instance with many viral illnesses. (Meaning, once you 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 ill and developed antibodies, only those antibodies were non the neutralizing kind, meaning the kind of antibodies that block infection. Equally a result, they were non protected from reinfection, and when exposed to MERS for a 2nd time, they became ill again, and more severely and then.

"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 second infection, preventing the animals from being infected a third fourth dimension. According to the authors:

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

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

And here'south an important point: COVID-19 vaccines are NOT designed to prevent infection. Every bit detailed in "How COVID-nineteen Vaccine Trials Are Rigged," a "successful" vaccine merely needs to reduce the severity of the symptoms. They're not fifty-fifty 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 April 2020:8

"The pathogenesis of COVID-19 is currently believed to go on via both directly cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent damage may involve the then-chosen antibiotic-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 simply for the understanding of viral pathogenesis, but 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, cross-neutralizing antibodies confronting different serotypes are brusk-lived and may last only upward to ii years.
In Dengue fever, reinfection with a different serotype runs a more than severe course 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 first infection.
Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the primary infection, the longer the filibuster to symptomatic secondary infection ..."

The paper goes on to item results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization charge per unit for Dengue among vaccinated children nether the age of 9 was greater than the charge per unit amid controls. The explanation for this appears to exist that the vaccine mimicked a primary infection, and every bit that immunity waned, the children became susceptible to ADE when they encountered the virus a second fourth dimension. The writer explains:

"A post 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 confronting astringent Dengue [in] those who had been exposed to the natural infection before vaccination, and that the gamble of severe clinical consequence 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 end up existence important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-ii works like Dengue, which is too caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually be at increased risk for severe COVID-19 subsequently vaccination, and merely those who have already recovered from a bout of COVID-19 would be protected against astringent affliction by the vaccine.

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

The Swiss Medical Weekly paper 9 also reviews the bear witness of ADE in coronavirus infections, citing enquiry showing inoculating cats against the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the disease when challenged with the same FIPV serotype every bit 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 newspaper 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 Confronting Fasten Proteins," published in 2014, found that:

"... college concentrations of anti-sera confronting 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 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 propose 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. Here, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike 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 damage, likely past "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Subsequently 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 at present fear, namely that COVID-xix vaccines may end upwardly making people more prone to astringent SARS-CoV-2 infection.

The newspaper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunopathology in one case challenged with the SARS virus. As noted past the authors: xiii

Inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-type immunopathologic in lungs after challenge.

As indicated, two reports attributed the immunopathology to presence of the N poly peptide in the vaccine; however, we found the same immunopathologic reaction in animals given Southward protein vaccine simply, although it appeared to be of bottom intensity.

Thus, a Th2-blazon immunopathologic reaction on challenge of vaccinated animals has occurred in three of four creature models (not in hamsters) including two different 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 result in mice, ferrets and nonhuman primates has not been reported.

This combined feel provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines accept been conducted and reported to induce antibiotic responses and to be 'safe.' However, the evidence for safety is for a short flow of observation.

The concern arising from the nowadays 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 safety against antigenic variants of SARS-CoV and for safety 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's bear witness showing the elderly — who are nearly vulnerable to severe COVID-19 — are besides the most vulnerable to ADE. Preliminary research findings14 posted on the preprint server medRxiv at the end of March 2020 reported that middle-anile and elderly COVID-xix patients accept far higher levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.


Immune Enhancement Is a Serious Concern

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 point out that:16

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-two are promising, they both pose a common theoretical prophylactic 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-2 infection ...
Immune enhancement of affliction tin theoretically occur in two ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-ii infection into target cells.
Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement furnishings are summarized in Fig. i ...
Currently, in that location are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early stage clinical trials. Brute studies on these CoVs have shown that the spike (S) protein-based vaccines (specifically the receptor bounden domain, RBD) are highly immunogenic and protective confronting wild-blazon CoV challenge.
Vaccines that target other parts of the virus, such as the nucleocapsid, without the South poly peptide, have shown no protection against CoV infection and increased lung pathology. However, immunization with some S protein based CoV vaccines accept too displayed signs of enhanced lung pathology following challenge.
Hence, besides the selection of antigen target, vaccine efficacy and risk of immunopathology may be dependent on other ancillary factors, including adjuvant conception, age at vaccination ... and road of immunization."

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

© articles.mercola.com
Figure 1: Mechanism of ADE and antibiotic mediated immunopathology. Left console: 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 crusade 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 Gamble-Benefit Analysis Before Making Up Your Mind

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

Ironically, the data 17,18,19 nosotros now accept no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60. 20 If you're nether the age of 40, your risk of dying from COVID-19 is just 0.01%, meaning you have a 99.99% chance of surviving the infection. And you could better that to 99.999% if you're metabolically flexible and vitamin D replete.

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

To circle back to where nosotros started, participants in current COVID-19 vaccine trials are non being told of this risk — that by getting the vaccine they may terminate up with more astringent COVID-nineteen one time they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Risk

In closing, consider what this PNAS news characteristic states well-nigh the adventure 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 equally dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) take shown a paradoxical miracle:
Some animals or people who received the vaccine and were afterward exposed to the virus developed more than severe affliction than those who had not been vaccinated. The vaccine-primed immune arrangement, in certain cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or and so-called allowed enhancement, may manifest in unlike ways such as antibiotic-dependent enhancement (ADE), a process in which a virus leverages antibodies to assist infection; or cell-based enhancement, a category that includes allergic inflammation caused past Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers debate that although ADE has received the virtually attention to date, it is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-nineteen, given what is known near the epidemiology of the virus and its behavior 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 Due north Carolina at Chapel Hill.
In previous studies of SARS, aged mice were found to have particularly 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 system and potentially dissentious the airways."


Sources and References

  • i International Periodical of Clinical Do, Oct 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
  • 3 Viral Immunology 2003;16(i):69-86
  • 4 Scientific discipline Straight Neutralizing Antibody
  • v Science Direct Binding Antibody
  • vi Twitter, The Immunologist Apr 9, 2020
  • 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
  • 8, 9 Swiss Medical Weekly April 16, 2020; 150:w20249
  • x Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(2): 208-214
  • 11 JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS Ane April 2012; 7(4): e35421 (PDF)
  • 13 PLOS I April 2012; 7(4): e35421 (PDF), page xi
  • 14 medRxiv DOI:10.1101/2020.03.30.20047365 (PDF)
  • xv EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Register of Internal Medicine September two, 2020 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, Dr., aprox 8 minutes in (Prevarication No. 1: Death Adventure)
  • 19 Technical Study June 2020 DOI: 10.13140/RG.ii.24350.77125