Covid Vaccine

© Image past Gerd Altmann from Pixabay

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 than astringent disease if they're exposed to the virus.

The written report,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Gamble of COVID-19 Vaccine Worsening Clinical Affliction," published in the International Periodical of Clinical Practice, Oct 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 non vaccinated."

"Vaccines for SARS, MERS and RSV have never been canonical, and the data generated in the evolution and testing of these vaccines suggest a serious mechanistic business organization: that vaccines designed empirically using the traditional arroyo (consisting of the unmodified or minimally modified coronavirus viral fasten 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 newspaper states.
"This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 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-19 take a chance of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well equally those beingness recruited for the trials and future patients after vaccine blessing, in order to encounter the medical ethics standard of patient comprehension for informed consent."


What Is Antibody-Dependent Enhancement?

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

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

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 beginning of this push for a COVID-xix vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Affliction" explains it this style:iii

"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 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 heighten 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 equally preferential replication in macrophages, ability to institute persistence, and antigenic diverseness. For some viruses, ADE of infection has become a dandy concern to illness 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 development, which began in 2002, following iii consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had near 30 promising candidates.

Of those, the four all-time vaccine candidates were so given to ferrets, which are the closest counterpart 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, one time 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 affliction that is very like to that caused past coronaviruses. At that time, they had decided to skip animate being trials and go directly to homo trials.

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


Neutralizing Versus Binding Antibodies

Coronaviruses produce not but one merely two unlike types of antibodies:

  • Neutralizing antibodies,4 also referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Bounden antibodies5 (as well known as non-neutralizing antibodies) that cannot forestall viral infection

Instead of preventing viral infection, bounden antibodies trigger an abnormal immune response known as "paradoxical immune enhancement." Another style to look at this is your immune system is actually backfiring and not functioning to protect you but actually 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 fasten protein (Due south protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the outset stage of the two-stage process viruses apply to gain entry into cells.

The thought is that by creating the SARS-CoV-2 fasten protein, your immune system will embark production of antibodies, without making you lot sick in the process. The key question is, which of the two types of antibodies are beingness produced through this procedure?


Without Neutralizing Antibodies, Wait More Severe Illness

In an April 2020 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering amnesty passports, we must starting time sympathize the complex role of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that have raised concerns most 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 Antibody," which investigated whether getting infected with MERS would protect the discipline 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 again.)

To make up one's mind how MERS affects the immune system, the researchers infected white rabbits with the virus. The rabbits got sick and developed antibodies, just those antibodies were not the neutralizing kind, significant the kind of antibodies that block infection. Every bit a upshot, they were not protected from reinfection, and when exposed to MERS for a second fourth dimension, they became ill once again, and more than 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 tertiary time. According to the authors:

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

In other words, if the vaccine does not result in a robust response in neutralizing antibodies, yous might exist at adventure for more than severe lung disease if y'all're infected with the virus.

And here'south an of import 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 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 April 2020:8

"The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and immune-mediated mechanisms. An boosted mechanism facilitating viral jail cell entry and subsequent harm may involve the so-called 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 phenomenon is of enormous relevance not only for the understanding of viral pathogenesis, but also 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 up to two years.
In Dengue fever, reinfection with a different serotype runs a more severe grade when the protective antibody titer wanes. Hither, non-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 dissimilar from the starting time infection.
Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the college the titer of such antibodies following the primary infection, the longer the filibuster to symptomatic secondary infection ..."

The newspaper goes on to detail results from follow-upwards 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 equally that immunity waned, the children became susceptible to ADE when they encountered the virus a 2nd time. The writer explains:

"A post hoc assay of efficacy trials, using an anti-nonstructural protein one immunoglobulin Chiliad (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 gamble of astringent clinical outcome was increased amid seronegative persons.
Based on this, a Strategic Advisor Group of Experts convened by Globe Health Arrangement (WHO) concluded that simply Dengue seropositive persons should exist vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could end upward being important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-ii works like Dengue, which is too acquired by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually exist at increased run a risk for astringent COVID-19 afterward vaccination, and only those who have already recovered from a bout of COVID-19 would exist protected against astringent illness by the vaccine.

To be articulate, we practise non know whether that is the case or non, merely these are important areas of inquiry and the current vaccine trials will simply non exist able to reply this of import question.

The Swiss Medical Weekly paper 9 too reviews the prove of ADE in coronavirus infections, citing research showing inoculating cats against the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the illness 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 newspaper likewise cites inquiry 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,x "Antibiotic-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against 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 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. We also generated monoclonal antibodies confronting SARS-CoV fasten proteins and observed that most of them promoted SARS-CoV infection.

Combined, our results advise that antibodies confronting SARS-CoV spike proteins may trigger ADE furnishings. The data enhance 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 concluded upward with more than 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 diffuse 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 fear, namely that COVID-19 vaccines may end upwards making people more decumbent to severe SARS-CoV-2 infection.

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

As indicated, two reports attributed the immunopathology to presence of the Northward protein in the vaccine; yet, we plant the same immunopathologic reaction in animals given South protein vaccine only, although it appeared to be of bottom intensity.

Thus, a Th2-blazon immunopathologic reaction on claiming of vaccinated animals has occurred in iii of four fauna models (non in hamsters) including two different inbred mouse strains with four dissimilar 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 feel 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.' All the same, the evidence for safety is for a curt period of observation.

The business concern arising from the present study is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional safe concerns relate to effectiveness and safety confronting antigenic variants of SARS-CoV and for condom 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's bear witness showing the elderly — who are most vulnerable to severe COVID-19 — are also the most vulnerable to ADE. Preliminary enquiry findingsxiv posted on the preprint server medRxiv at the end of March 2020 reported that middle-anile and elderly COVID-xix patients have 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." Equally in many other papers, the authors betoken out that:16

"While evolution of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical safety concern. Experimental studies accept suggested the possibility of immune-enhanced illness of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-two infection ...
Allowed enhancement of disease can 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 heighten inflammation and hence severity of pulmonary affliction. An overview of these antibody 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. Beast studies on these CoVs have shown that the fasten (Due south) protein-based vaccines (specifically the receptor bounden domain, RBD) are highly immunogenic and protective against wild-type CoV challenge.
Vaccines that target other parts of the virus, such as the nucleocapsid, without the S protein, accept shown no protection against CoV infection and increased lung pathology. Yet, immunization with some S protein based CoV vaccines take also displayed signs of enhanced lung pathology following challenge.
Hence, also the choice of antigen target, vaccine efficacy and risk 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

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


Do a Chance-Do good Assay Before Making Up Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines finish upwardly being, they'll be released to the public in relatively brusk society. Most predict one or more vaccines will be ready onetime in 2021.

Ironically, the information 17,18,19 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 age of sixty. xx If you're under the age of twoscore, your gamble of dying from COVID-19 is merely 0.01%, meaning y'all have a 99.99% chance of surviving the infection. And you could ameliorate that to 99.999% if you're metabolically flexible and vitamin D replete.

And so, really, what are nosotros protecting against with a COVID-xix vaccine? As mentioned, the vaccines aren't even designed to preclude infection, only 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 risk 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 take a chance — that past getting the vaccine they may cease upwardly with more severe COVID-nineteen once they're infected with the virus.


Lethal Th2 Immunopathology Is Some other Potential Risk

In closing, consider what this PNAS news characteristic states about the hazard of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offering the near:21

"Since the 1960s, tests of vaccine candidates for diseases such every bit dengue, respiratory syncytial virus (RSV), and astringent astute respiratory syndrome (SARS) have shown a paradoxical phenomenon:
Some animals or people who received the vaccine and were later exposed to the virus developed more severe 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 so-chosen immune enhancement, may manifest in unlike ways such as antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to aid infection; or prison cell-based enhancement, a category that includes allergic inflammation acquired past Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers argue that although ADE has received the about attending to date, it is less probable than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known most the epidemiology of the virus and its beliefs in the homo body.
'There is the potential for ADE, but the bigger trouble is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and good in coronaviruses ... at the Academy of Northward Carolina at Chapel Hill.
In previous studies of SARS, anile mice were found to accept particularly high risks of life-threatening Th2 immunopathology ... in which a faulty T jail cell response triggers allergic inflammation, and poorly functional antibodies that form immune complexes, activating the complement system and potentially damaging the airways."


Sources and References

  • 1 International Periodical of Clinical Do, October 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (xv) 8218-8221
  • 3 Viral Immunology 2003;16(1):69-86
  • 4 Scientific discipline Straight Neutralizing Antibody
  • 5 Science Straight Binding Antibody
  • 6 Twitter, The Immunologist April 9, 2020
  • seven PLOS Pathogens 2017 Aug; xiii(8): e1006565
  • 8, nine Swiss Medical Weekly Apr xvi, 2020; 150:w20249
  • 10 Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(two): 208-214
  • 11 JCI Insight February 21, 2019 DOI: x.1172/jci.insight.123158
  • 12 PLOS ONE Apr 2012; 7(4): e35421 (PDF)
  • 13 PLOS ONE April 2012; 7(4): e35421 (PDF), page eleven
  • 14 medRxiv DOI:ten.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, twenty Annals of Internal Medicine September ii, 2020 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the ascension of medical technocracy, Lee Merritt, Doc, aprox 8 minutes in (Lie No. i: Death Adventure)
  • 19 Technical Report June 2020 DOI: x.13140/RG.2.24350.77125