Covid Vaccine

© Image past Gerd Altmann from Pixabay

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

The written report,1 "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Disease," published in the International Journal of Clinical Practice, October 28, 2020, points out that "COVID-19 vaccines designed to arm-twist neutralizing antibodies may sensitize vaccine recipients to more astringent disease than if they were non vaccinated."

"Vaccines for SARS, MERS and RSV accept 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 equanimous of poly peptide, viral vector, Dna or RNA and irrespective of delivery method, may worsen COVID-19 affliction via antibody-dependent enhancement (ADE)," the paper 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 chance is unlikely to occur, obviating truly informed consent by subjects in these trials.
The specific and significant COVID-nineteen risk of ADE should accept been and should be prominently and independently disclosed to enquiry subjects currently in vaccine trials, as well every bit those being recruited for the trials and future patients after vaccine approval, in lodge to meet the medical ethics standard of patient comprehension for informed consent."


What Is Antibiotic-Dependent Enhancement?

Every bit noted past the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for astringent astute respiratory syndrome coronavirus (SARS-CoV), Center East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious business concern: The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that hateful? In a nutshell, it ways 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 severe disease than had you not been vaccinated. 2

This is the exact reverse of what a vaccine is supposed to do, and a significant problem that has been pointed out from the very start of this push for a COVID-nineteen vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Illness" 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 means. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This activity is known as antibody-dependent enhancement (ADE) of virus infection.
The ADE of virus infection is a phenomenon in which virus-specific antibodies enhance the entry of virus, and in some cases the replication of virus, into monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors.
This miracle 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 diversity. For some viruses, ADE of infection has become a great concern to affliction 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 development, which began in 2002, following three consecutive SARS outbreaks. Past 2012, Chinese, American and European scientists were working on SARS vaccine development, and had about 30 promising candidates.

Of those, the iv best vaccine candidates were then 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 antibiotic response, which is the metric used for vaccine licensing, once they were challenged with the wild virus, they all became severely sick 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 by coronaviruses. At that time, they had decided to skip animate being trials and go directly to human trials.

"They tested it on I call back 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 sick. Ii of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH."


Neutralizing Versus Binding Antibodies

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

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

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

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

The idea is that past creating the SARS-CoV-two fasten protein, your immune system volition commence product of antibodies, without making you sick in the process. The central question is, which of the two types of antibodies are being produced through this procedure?


Without Neutralizing Antibodies, Expect More than Severe Illness

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

The commencement 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 discipline confronting reinfection, as is typically the case with many viral illnesses. (Significant, once yous recover from a viral infection, say measles, y'all're allowed and won't contract the illness over again.)

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 not the neutralizing kind, pregnant the kind of antibodies that cake infection. Equally a result, they were not protected from reinfection, and when exposed to MERS for a second time, they became sick 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 second 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 neglect to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at hazard for severe lung disease on re-exposure to MERS-CoV."

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

And here'south an important point: COVID-nineteen vaccines are Non designed to prevent infection. As detailed in "How COVID-19 Vaccine Trials Are Rigged," a "successful" vaccine just 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 as well known to cause ADE. As explained in a Swiss Medical Weekly newspaper published in April 2020:8

"The pathogenesis of COVID-xix is currently believed to proceed via both straight cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent damage may involve the then-called 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 non only for the understanding of viral pathogenesis, merely besides for developing antiviral strategies, notably vaccines ...
At that place are iv serotypes of Dengue virus, all eliciting protective immunity. Nevertheless, although homotypic protection is long-lasting, cantankerous-neutralizing antibodies confronting dissimilar serotypes are short-lived and may concluding only up to 2 years.
In Dengue fever, reinfection with a dissimilar serotype runs a more astringent course when the protective antibiotic titer wanes. Here, 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 unlike from the offset infection.
Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the main infection, the longer the delay to symptomatic secondary infection ..."

The paper goes on to detail results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization charge per unit for Dengue among vaccinated children under the historic period of 9 was greater than the rate among controls. The explanation for this appears to exist that the vaccine mimicked a primary infection, and as that immunity waned, the children became susceptible to ADE when they encountered the virus a 2d time. The author explains:

"A postal service hoc assay of efficacy trials, using an anti-nonstructural protein i immunoglobulin Thousand (IgG) enzyme-linked immunosorbent analysis (ELISA) to distinguish antibodies elicited past wild-blazon 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 risk 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 command programs are planned that include vaccination."

ADE in Coronavirus Infections

This could stop up existence important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-two works like Dengue, which is also acquired past an RNA virus, and then anyone who has not tested positive for SARS-CoV-2 might actually exist at increased risk for severe COVID-19 after vaccination, and only those who have already recovered from a bout of COVID-nineteen would be protected against astringent affliction by the vaccine.

To exist clear, we do non know whether that is the case or not, just 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 evidence 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 disease when challenged with the same FIPV serotype as that in the vaccine.

Experiments have shown immunization with a diversity of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The newspaper also cites enquiry showing "Antibodies elicited by a SARS-CoV vaccine enhanced infection of B cell lines in spite of protective responses in the hamster model." Another paper,ten "Antibiotic-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. We too generated monoclonal antibodies against SARS-CoV spike proteins and observed that nearly of them promoted SARS-CoV infection.

Combined, our results suggest that antibodies against SARS-CoV spike proteins may trigger ADE effects. The information 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 fasten poly peptide concluded up 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 adult astute diffuse alveolar damage, probable past "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Afterwards Claiming With SARS-CoV

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

The paper reviews experiments showing immunization with a diversity 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 subsequently claiming.

As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; however, we constitute the same immunopathologic reaction in animals given S protein vaccine merely, although it appeared to be of bottom intensity.

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

This combined experience provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines have been conducted and reported to induce antibody responses and to be 'safety.' Nevertheless, the evidence for safety is for a short period of ascertainment.

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


The Elderly Are Most Vulnerable to ADE

On superlative of all of these concerns, there's testify showing the elderly — who are nigh vulnerable to severe COVID-xix — are too the most vulnerable to ADE. Preliminary inquiry findingsxiv posted on the preprint server medRxiv at the terminate of March 2020 reported that eye-aged and elderly COVID-19 patients have far higher levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.


Allowed 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 Evolution." Equally in many other papers, the authors bespeak out that:xvi

"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 have suggested the possibility of immune-enhanced affliction 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 two ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-2 infection into target cells.
Secondly, antibodies could heighten inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. 1 ...
Currently, in that location are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animate being studies on these CoVs have shown that the spike (Southward) 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 every bit the nucleocapsid, without the S protein, have shown no protection against CoV infection and increased lung pathology. Yet, immunization with some S protein based CoV vaccines have likewise displayed signs of enhanced lung pathology post-obit challenge.
Hence, too 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 road of immunization."

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

© manufactures.mercola.com
Figure 1: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex internalization is mediated by the date of activating Fc receptors on the jail 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 allowed activation results in the release of cytokines and chemokines, leading to enhanced illness pathology.


Practice a Risk-Benefit Analysis Before Making Upwardly Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines terminate upward being, they'll be released to the public in relatively short order. Virtually predict one or more vaccines volition be set sometime 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 influenza for those under the age of 60. 20 If you're under the age of 40, your adventure of dying from COVID-19 is just 0.01%, pregnant y'all have a 99.99% hazard of surviving the infection. And you could improve that to 99.999% if you lot'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, but reduce the severity of symptoms. Meanwhile, they could potentially make you lot sicker in one case y'all'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 beingness told of this hazard — that past getting the vaccine they may cease upwardly with more than severe COVID-19 once they're infected with the virus.


Lethal Th2 Immunopathology Is Another Potential Take chances

In closing, consider what this PNAS news feature states about the take chances of vaccine-induced allowed enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offering the most:21

"Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe 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 than astringent disease than those who had not been vaccinated. The vaccine-primed immune system, in sure cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or and so-chosen immune enhancement, may manifest in different means such as antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to assistance infection; or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes might overlap ...
Some researchers fence that although ADE has received the about attention to engagement, it is less likely than the other immune enhancement pathways to crusade a dysregulated response to COVID-19, given what is known near the epidemiology of the virus and its behavior in the human torso.
'At that place is the potential for ADE, but the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the Academy of North Carolina at Chapel Colina.
In previous studies of SARS, aged mice were plant 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 allowed complexes, activating the complement system and potentially dissentious the airways."


Sources and References

  • ane International Journal of Clinical Practice, Oct 28, 2020 DOI: 10.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2020 117 (fifteen) 8218-8221
  • 3 Viral Immunology 2003;16(i):69-86
  • four Scientific discipline Directly Neutralizing Antibiotic
  • v Science Direct Binding Antibiotic
  • 6 Twitter, The Immunologist April nine, 2020
  • vii PLOS Pathogens 2017 Aug; 13(eight): e1006565
  • 8, ix Swiss Medical Weekly April 16, 2020; 150:w20249
  • x Biochemical and Biophysical Inquiry Communications August 22, 2014; 451(two): 208-214
  • 11 JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
  • 12 PLOS ONE Apr 2012; 7(4): e35421 (PDF)
  • thirteen PLOS 1 Apr 2012; 7(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:ten.1101/2020.03.30.20047365 (PDF)
  • 15 EBioMedicine 2020 May; 55: 102768
  • 16 EBioMedicine 2020 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September 2, 2020 DOI: x.7326/M20-5352
  • 18 YouTube, SARS-CoV-ii and the rise of medical technocracy, Lee Merritt, MD, aprox eight minutes in (Lie No. i: Expiry Take chances)
  • 19 Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125