Covid Vaccine

© Image by 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 severe 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 Illness," published in the International Journal of Clinical Do, October 28, 2022, points out that "COVID-xix vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe illness than if they were non vaccinated."

"Vaccines for SARS, MERS and RSV take 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 arroyo (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), be they composed of protein, viral vector, DNA or RNA and irrespective of commitment method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE)," the paper states.
"This gamble 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 meaning COVID-19 hazard of ADE should have been and should be prominently and independently disclosed to enquiry subjects currently in vaccine trials, as well as those being recruited for the trials and future patients subsequently vaccine blessing, in lodge to meet the medical ideals standard of patient comprehension for informed consent."


What Is Antibody-Dependent Enhancement?

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

What exactly does that mean? In a nutshell, it 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 astringent illness than had yous not been vaccinated. two

This is the exact opposite of what a vaccine is supposed to do, and a pregnant problem that has been pointed out from the very starting time of this push for a COVID-19 vaccine. The 2003 review newspaper "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 ways. Notwithstanding, 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 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 mutual features such as preferential replication in macrophages, ability to institute persistence, and antigenic diverseness. For some viruses, ADE of infection has go a great business concern to disease control by vaccination."


Previous Coronavirus Vaccine Efforts Take All Failed

In my May 2022 interview above with Robert Kennedy Jr., he summarized the history of coronavirus vaccine development, which began in 2002, following three consecutive SARS outbreaks. By 2022, Chinese, American and European scientists were working on SARS vaccine development, and had about 30 promising candidates.

Of those, the four best vaccine candidates were then given to ferrets, which are the closest analogue to human 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 sick and died.

The same matter happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory illness that is very like to that acquired by coronaviruses. At that time, they had decided to skip animal trials and go direct to human trials.

"They tested it on I recollect near 35 children, and the same matter happened," Kennedy said. "The children developed a champion antibody response — robust, durable. It looked perfect [but when] the children were exposed to the wild virus, they all became sick. Two of them died. They abandoned the vaccine. It was a large embarrassment to FDA and NIH."


Neutralizing Versus Bounden Antibodies

Coronaviruses produce non merely ane only two different types of antibodies:

  • Neutralizing antibodies,4 also referred to as immunoglobulin G (IgG) antibodies, that fight the infection
  • Binding antibodiesfive (as well known equally non-neutralizing antibodies) that cannot preclude viral infection

Instead of preventing viral infection, binding antibodies trigger an abnormal allowed response known equally "paradoxical immune enhancement." Another way to look at this is your immune arrangement is really backfiring and not functioning to protect y'all but 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 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-stage process viruses employ to gain entry into cells.

The idea is that by creating the SARS-CoV-ii spike protein, your allowed system will commence product of antibodies, without making you ill in the process. The key question is, which of the two types of antibodies are beingness produced through this process?


Without Neutralizing Antibodies, Await More than Severe Illness

In an April 2022 Twitter thread,6 The Immunologist noted: "While developing vaccines ... and considering immunity passports, we must first empathize the complex part of antibodies in SARS, MERS and COVID-19." He goes on to list several coronavirus vaccine studies that have raised concerns virtually ADE.

The offset is a 2022 study7 in PLOS Pathogens, "Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absence of Neutralizing Antibiotic," which investigated whether getting infected with MERS would protect the subject against reinfection, equally is typically the case with many viral illnesses. (Pregnant, one time y'all recover from a viral infection, say measles, you lot're immune and won't contract the illness again.)

To determine how MERS affects the immune organization, the researchers infected white rabbits with the virus. The rabbits got sick and adult antibodies, just those antibodies were non the neutralizing kind, meaning the kind of antibodies that cake infection. As a result, they were not protected from reinfection, and when exposed to MERS for a second 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 2nd infection, preventing the animals from existence infected a third time. 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 accept waned, may be at risk for severe lung disease on re-exposure to MERS-CoV."

In other words, if the vaccine does not result in a robust response in neutralizing antibodies, you might exist at take chances for more than severe lung disease if you lot're infected with the virus.

And hither's an important point: COVID-nineteen vaccines are Not designed to prevent infection. Equally detailed in "How COVID-xix Vaccine Trials Are Rigged," a "successful" vaccine merely needs to reduce the severity of the symptoms. They're not even looking at reducing infection, hospitalization or decease rates.

ADE in Dengue Infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly newspaper published in April 2022:eight

"The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and allowed-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent impairment 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, merely also for developing antiviral strategies, notably vaccines ...
There are 4 serotypes of Dengue virus, all eliciting protective immunity. Nonetheless, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may last but up to ii years.
In Dengue fever, reinfection with a different serotype runs a more severe form when the protective antibody titer wanes. Here, 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 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 detail results from follow-upwardly investigations into the Dengue vaccine, which revealed the hospitalization charge per unit for Dengue among vaccinated children under the age of nine was greater than the charge per unit 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 second fourth dimension. The writer explains:

"A postal service hoc assay of efficacy trials, using an anti-nonstructural protein i immunoglobulin Thousand (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited past wild-type 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 severe clinical effect was increased among seronegative persons.
Based on this, a Strategic Advisor Grouping of Experts convened past World Health Organisation (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 end up 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 not tested positive for SARS-CoV-2 might actually be at increased gamble for astringent COVID-nineteen after vaccination, and only those who accept already recovered from a bout of COVID-xix would be protected confronting severe illness by the vaccine.

To be clear, we exercise not know whether that is the example or not, just these are important areas of research and the current vaccine trials will but non be able to respond this of import question.

The Swiss Medical Weekly paper nine also reviews the testify 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 equally that in the vaccine.

Experiments have shown immunization with a variety of SARS vaccines resulted in pulmonary immunopathology one time challenged with the SARS virus.

The paper too 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 paper,10 "Antibiotic-Dependent SARS Coronavirus Infection Is Mediated past Antibodies Against Spike Proteins," published in 2022, 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 past diluted antibodies confronting envelope spike proteins rather than nucleocapsid proteins. We besides generated monoclonal antibodies against SARS-CoV spike proteins and observed that about of them promoted SARS-CoV infection.

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

A reportxi that ties into this was published in the journal JCI Insight in 2022. Hither, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV fasten 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 developed astute diffuse alveolar damage, probable by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Later on Challenge With SARS-CoV

An interesting 2022 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 than prone to severe SARS-CoV-two infection.

The paper reviews experiments showing immunization with a diversity of SARS vaccines resulted in pulmonary immunopathology in one case challenged with the SARS virus. As 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-type immunopathologic in lungs later challenge.

As indicated, 2 reports attributed the immunopathology to presence of the N poly peptide in the vaccine; however, nosotros plant the aforementioned immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity.

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in iii of four animal models (not in hamsters) including two dissimilar inbred mouse strains with four unlike 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 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 'condom.' Nevertheless, the evidence for safety is for a short period of ascertainment.

The business organization 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. Boosted safe concerns relate to effectiveness and prophylactic against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, particularly those of the type 2 group."


The Elderly Are Most Vulnerable to ADE

On top of all of these concerns, there'due south evidence showing the elderly — who are most vulnerable to severe COVID-nineteen — are besides the most vulnerable to ADE. Preliminary enquiry findings14 posted on the preprint server medRxiv at the end of March 2022 reported that eye-anile and elderly COVID-19 patients have far college levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.


Immune Enhancement Is a Serious Concern

Some other paper worth mentioning is the May 2022 mini review15 "Impact of Allowed 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-2 are promising, they both pose a common theoretical safety business organization. Experimental studies accept suggested the possibility of immune-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-two infection ...
Allowed enhancement of affliction tin theoretically occur in 2 ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies tin can heighten SARS-CoV-ii infection into target cells.
Secondly, antibodies could raise inflammation and hence severity of pulmonary disease. An overview of these antibody 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 fasten (S) poly peptide-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective against wild-blazon CoV challenge.
Vaccines that target other parts of the virus, such as the nucleocapsid, without the S protein, have shown no protection confronting CoV infection and increased lung pathology. However, immunization with some S poly peptide based CoV vaccines have also displayed signs of enhanced lung pathology post-obit challenge.
Hence, as well the selection of antigen target, vaccine efficacy and risk of immunopathology may be dependent on other ancillary factors, including adjuvant conception, historic period at vaccination ... and route of immunization."

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

© articles.mercola.com
Figure ane: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, allowed 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 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.


Practice a Risk-Benefit Analysis Before Making Up Your Listen

In all likelihood, regardless of how constructive (or ineffective) the COVID-19 vaccines end up being, they'll be released to the public in relatively short order. Near predict one or more vaccines will exist ready sometime in 2022.

Ironically, the information 17,18,19 we at present have no longer back up a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the historic period of 60. 20 If you're under the historic period of 40, your risk of dying from COVID-19 is just 0.01%, meaning you have a 99.99% gamble of surviving the infection. And you could ameliorate that to 99.999% if you're metabolically flexible and vitamin D replete.

So, really, what are we protecting confronting with a COVID-19 vaccine? As mentioned, the vaccines aren't fifty-fifty 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 take chances for a truly questionable benefit.

To circle back to where nosotros started, participants in electric current COVID-19 vaccine trials are not existence told of this risk — that past getting the vaccine they may finish 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 gamble of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offer the virtually: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 phenomenon:
Some animals or people who received the vaccine and were later exposed to the virus adult more astringent affliction than those who had not been vaccinated. The vaccine-primed allowed arrangement, in certain cases, seemed to launch a shoddy response to the natural infection ...
This immune backfiring, or so-chosen immune enhancement, may manifest in different ways such every bit antibody-dependent enhancement (ADE), a procedure in which a virus leverages antibodies to help 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 argue that although ADE has received the most attending to date, it is less likely than the other allowed enhancement pathways to cause a dysregulated response to COVID-xix, given what is known about the epidemiology of the virus and its behavior in the man body.
'In that location is the potential for ADE, but the bigger trouble is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and adept in coronaviruses ... at the University of North Carolina at Chapel Hill.
In previous studies of SARS, aged mice were institute to accept particularly 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 organization and potentially damaging the airways."


Sources and References

  • 1 International Periodical of Clinical Practise, October 28, 2022 DOI: ten.111/ijcp.13795
  • 2, 21 PNAS.org April 14, 2022 117 (15) 8218-8221
  • iii Viral Immunology 2003;16(1):69-86
  • four Science Directly Neutralizing Antibiotic
  • 5 Science Direct Binding Antibody
  • half dozen Twitter, The Immunologist Apr 9, 2022
  • 7 PLOS Pathogens 2022 Aug; 13(8): e1006565
  • 8, 9 Swiss Medical Weekly April 16, 2022; 150:w20249
  • 10 Biochemical and Biophysical Research Communications Baronial 22, 2022; 451(two): 208-214
  • 11 JCI Insight February 21, 2022 DOI: x.1172/jci.insight.123158
  • 12 PLOS ONE Apr 2022; 7(four): e35421 (PDF)
  • thirteen PLOS ONE Apr 2022; 7(4): e35421 (PDF), page 11
  • 14 medRxiv DOI:ten.1101/2020.03.xxx.20047365 (PDF)
  • fifteen EBioMedicine 2022 May; 55: 102768
  • 16 EBioMedicine 2022 May; 55: 102768, Introduction
  • 17, 20 Annals of Internal Medicine September 2, 2022 DOI: 10.7326/M20-5352
  • 18 YouTube, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, Md, aprox 8 minutes in (Lie No. 1: Death Risk)
  • xix Technical Report June 2022 DOI: 10.13140/RG.2.24350.77125