How does the COVID-19 Vaccine Destroy Your Immune System?


According to a study examining how informed consent is given to participants in a COVID-19 vaccine trial, the information forms do not tell volunteers that the vaccine could make them more susceptible to more severe illness if they are exposed to the virus.

Vaccines for SARS, MERS, and RSV have never been Licensed

The study, “Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Disease,” published Oct. 28, 2020, in the International Journal of Clinical Practice, notes that “COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated.”

Vaccines against SARS, MERS, and RSV have never been licensed, and data generated during the development and testing of these vaccines suggest a serious mechanistic problem: That vaccines developed empirically using the traditional approach (consisting of the unaltered or minimally altered viral coronavirus spike to elicit neutralizing antibodies), regardless of whether they consist of a protein, viral vector, DNA, or RNA, and regardless of the delivery method, can exacerbate COVID-19 disease through 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 patients are unlikely to adequately understand this risk, which prevents truly informed consent from subjects in these trials.

The specific and significant COVID-19 risk of ADE should be prominently and independently disclosed to subjects currently participating in the vaccine trials, as well as to those being recruited for the trials and to prospective patients once the vaccine is approved, in order to meet the medical ethics standard of patient understanding for informed consent.

What is Antibody-Dependent Enhancement?

As the authors of the article in the International Journal of Clinical Practice note, previous efforts to vaccinate against coronaviruses-severe acute respiratory syndrome (SARS-CoV), Middle East coronavirus (MERS-CoV), and respiratory syncytial virus (RSV)-have raised a serious issue: The vaccines have a tendency to trigger antibody-dependent boosting.

What exactly does this mean? In short, it means that the vaccine does not boost your immunity to the infection, but rather enhances the ability of the virus to enter and infect your cells, resulting in a more severe illness than if you had not been vaccinated.

This is the exact opposite of what a vaccine is supposed to do, and a significant problem that has been pointed out from the beginning in connection with the call for a COVID-19 vaccine. The 2003 review paper “Antibody-Dependent Enhancement of Virus Infection and Disease” explains this as follows:

In general, virus-specific antibodies are considered antiviral and play an important role in controlling viral infections in several ways. However, in some cases, the presence of specific antibodies may also be beneficial to the virus. This activity is referred to as antibody-dependent enhancement (ADE) of viral infection.

ADE of viral infection is a phenomenon in which virus-specific antibodies promote viral entry and, in some cases, viral replication in monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors.

This phenomenon has been observed in vitro and in vivo in viruses of numerous families and genera of public health and veterinary importance. These viruses share some common features, such as preferential replication in macrophages, the ability to persist, and antigenic diversity. For some viruses, ADE of infection has become a major problem for disease control through vaccination.

Previous Efforts at a Coronavirus Vaccine Have All Failed

In my May 2020 interview above with Robert Kennedy Jr. he summarized the history of coronavirus vaccine development that began in 2002 after three consecutive SARS outbreaks. By 2012, Chinese, U.S., and European scientists were working on SARS vaccine development and had about 30 promising candidates.

Of these, the top four vaccine candidates were fed to ferrets, the closest to a human lung infection. In the video below, which is an excerpt from my full interview, Kennedy explains what happened next. While the ferrets showed a robust antibody response that serves as a benchmark for vaccine approval, they all became severely ill and died as soon as they were exposed to the wild virus.

The same thing happened when attempts were made to develop an RSV vaccine in the 1960s. RSV is an upper respiratory disease very similar to that caused by coronavirus. At that time, they had decided to skip animal testing and go directly to human trials.

They tested it on about 35 children, and the same thing happened,” Kennedy said. “The children developed an excellent antibody response – robust and durable. It looked perfect, but when the kids were exposed to the wild virus, they all got sick. Two of them died. The vaccine was abandoned. It was a huge embarrassment for the FDA and the NIH.

Neutralizing versus Binding Antibodies

Coronaviruses produce not one, but two different types of antibodies:

  • Neutralizing antibodies, also called immunoglobulin G (IgG) antibodies, which fight infection.
  • Binding antibodies (also called non-neutralizing antibodies), which cannot prevent viral infection

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response called “paradoxical immune enhancement.” You can also think of it as your immune system actually firing in the wrong direction, not protecting you but actually making you worse.

Pfizer and Moderna’s COVID-19 vaccines use mRNA to instruct your cells to make the SARS-CoV-2 spike protein (S protein). The spike protein, which attaches to the cell’s ACE2 receptor, is the first step in the two-step process by which viruses enter cells.

The idea is that by creating the SARS-CoV-2 spike protein, your immune system will start producing antibodies without making you sick. The key question is: Which of the two types of antibodies are produced by this process?

Without neutralizing Antibodies, more severe Disease is to be expected

In an April 2020 Twitter thread, The Immunologist noted, “In developing vaccines … and considering immune passports, we must first understand the complex role of antibodies in SARS, MERS, and COVID-19.” They list several coronavirus vaccine studies that have raised concerns about ADE.

The first is a 2017 study published in PLOS Pathogens titled “Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absence of Neutralizing Antibody,” which examined whether infection with MERS would protect the subject from reinfection, as is the case with many viral diseases. (That is, once you recover from a viral infection, such as measles, you are immune and will not get the disease again).

To determine how MERS affects the immune system, the researchers infected white rabbits with the virus. The rabbits became ill and developed antibodies, but these antibodies were not neutralizing, the type of antibodies that prevent infection. As a result, they were not protected from reinfection, and when they were exposed to the MERS virus a second time, they became ill again, and to an even greater degree.

“In fact, reinfection resulted in increased pneumonia without any increase in viral RNA titers,” the authors said. Interestingly, this second infection produced neutralizing antibodies that prevented the animals from being infected a third time. The authors write in response:

Our data from the rabbit model suggest that people who have been exposed to MERS-CoV and do not develop a neutralizing antibody response, or individuals whose neutralizing antibody titers have decayed, are at risk for severe lung disease if re-exposed to MERS-CoV

In other words: If the vaccine does not result in a robust response in the form of neutralizing antibodies, there is a risk of more severe lung disease if the virus is re-infected.

And this is an important point: the COVID-19 vaccines were NOT designed to prevent infection. By the manufacturers’ definition, a “successful” vaccine must only reduce the severity of symptoms.

ADE in Dengue Infections

Dengue virus can also cause ADE. As explained in an April 2020 publication of the Swiss Medical Weekly:

COVID-19 pathogenesis is currently thought to occur via both direct cytotoxic and immune-mediated mechanisms. An additional mechanism that facilitates viral entry into the cell and subsequent damage could be so-called antibody-dependent enhancement (ADE).

ADE is a very well-known cascade of events in which viruses can infect susceptible cells via the interaction between virions complexed with antibodies or complement components and Fc or complement receptors, leading to enhancement of their replication.

This phenomenon is of enormous importance not only for the understanding of viral pathogenesis but also for the development of antiviral strategies, especially vaccines …

There are four serotypes of dengue virus, all of which elicit protective immunity. However, while homotypic protection is long-lasting, cross-neutralizing antibodies to different serotypes are short-lived and can last only up to 2 years.

In dengue fever, reinfection with a different serotype is more severe when the protective antibody titer wanes. Here, non-neutralizing antibodies take over from neutralizing ones, bind to dengue viruses, and these complexes mediate infection of phagocytic cells by interacting with the Fc receptor in a typical ADE.

In other words, heterotypic antibodies with subneutralizing titers are responsible for ADEs in individuals infected with a different serotype of dengue virus than at initial infection.

Cross-reactive neutralizing antibodies are associated with a lower likelihood of symptomatic secondary infection, and the higher the titer of such antibodies after primary infection, the longer it takes for symptomatic secondary infection to occur …

The paper also lists the results of follow-up studies of the dengue vaccine, which showed that the hospitalization rate for dengue was higher in vaccinated children younger than 9 years than in the control group. The explanation appears to be that the vaccine mimics a primary infection, and as that immunity wears off, children become susceptible to ADE when they come into contact with the virus a second time. The author explains:

A post-hoc analysis of efficacy trials using an enzyme-linked immunosorbent assay (ELISA) against anti-structural protein 1 (IgG) to distinguish between antibodies elicited by wild-type infection and those that occur after vaccination showed that the vaccine could protect against severe dengue fever when children were exposed to natural infection before vaccination and that the risk of a severe clinical course was increased in seronegative individuals.

On this basis, a strategic expert group convened by the World Health Organization (WHO) concluded that only seropositive dengue patients should be vaccinated if dengue control programs are planned that include vaccination.

ADE in Coronavirus Infections

When researchers eventually evaluate how COVID-19 vaccines have worked so far, it could be significant for the COVID-19 vaccine.

Hypothetically speaking: If SARS-CoV-2 works like dengue, which is also 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 infection after vaccination, and only those who have already recovered from a COVID-19 attack would be protected from severe disease by the vaccine. These are important areas of investigation, and current vaccine trials simply will not answer this important question.

The Swiss Medical Weekly also reviews the evidence for ADE in coronavirus infections, citing research showing that vaccinating cats against feline infectious peritonitis virus (FIPV)-a feline coronavirus-increases disease severity when challenged with the same FIPV serotype as the vaccine.

Experiments have shown that immunization with different SARS vaccines leads to pulmonary immunophathology once exposed to the SARS virus.

The paper also cites research showing that “antibodies elicited by a SARS-CoV vaccine enhance infection of B-cell lineages despite protective responses in a hamster model.” Another study, titled “Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins,” published in 2014, found that:

“… higher concentrations of antisera against SARS-CoV neutralized SARS-CoV infection, whereas highly diluted antisera significantly increased SARS-CoV infection and induced higher levels of apoptosis.

The results of the infectivity assays suggest that ADE of SARS-CoV is mediated primarily by dilute antibodies to envelope spike proteins rather than nucleocapsid proteins. We also raised monoclonal antibodies against SARS-CoV spike proteins and found that most of them promote SARS-CoV infection.

Taken together, our results suggest that antibodies against SARS-CoV spike proteins can induce ADE effects. The data raise new questions with regard to a potential SARS-CoV vaccine …

A related study was published in 2019 in the journal JCI Insight. Macaques vaccinated with a modified vaccinia ankara virus (MVA) encoding the full-length SARS-CoV spike protein showed more severe lung pathology when the animals were exposed to the SARS virus. And when they transferred anti-spike IgG antibodies to unvaccinated macaques, the macaques developed acute diffuse alveolar damage, likely due to “distortion of the anti-inflammatory response.”

SARS vaccine exacerbates infection after challenge with SARS-CoV

An interesting 2012 paper with the telling title “Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus” shows what many researchers now fear, that COVID-19 vaccines may increase susceptibility to severe SARS-CoV-2 infection.

The paper examines experiments showing that immunization with various SARS vaccines leads to pulmonary immunophathology once exposed to SARS virus. The authors state:

Inactivated whole-virus vaccines, whether inactivated with formalin or beta-propiolactone and whether administered with or without alum adjuvant, resulted in Th2-type immunopathology in the lungs after infection.

As noted above, two reports attributed the immunopathology to the presence of the N protein in the vaccine; however, we found the same immunopathologic response in animals that received only the S protein vaccine, although it appeared to be of lesser intensity.

Thus, in three of four animal models (not hamsters), including two different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant, a Th2-type immunopathologic response was observed when vaccinated animals were provoked. An inactivated vaccine preparation that does not elicit this result in mice, ferrets, and nonhuman primates is not known.

These combined experiences raise concerns for human trials of SARS-CoV vaccines. Clinical trials of SARS coronavirus vaccines have been conducted and reported to elicit antibody responses and to be “safe.” However, the evidence for safety is for only a short observation period.

This report raises concerns that immunopathologic responses may occur in vaccinated individuals following exposure to infectious SARS-CoV, the basis for the development of a vaccine against SARS. Other safety concerns include efficacy and safety against antigenic variants of SARS-CoV and the safety of vaccinated persons exposed to other coronaviruses, particularly those in the type 2 group.

Elderly People are most Susceptible to ADEs

In addition to all of these concerns, evidence suggests that older people-who are most vulnerable to severe COVID-19-are also most vulnerable to ADE. Preliminary research published in late March 2020 on the preprint server medRxiv reports that middle-aged and elderly COVID-19 patients have much higher levels of anti-spike antibodies-which in turn increase infectivity-than younger patients.

Immune Boosting is a Serious Problem

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

The development of hyperimmune globulin therapy and a vaccine against SARS-CoV-2, while promising, also poses a common theoretical safety problem. Experimental studies have raised the possibility of immune-enhanced disease in SARS-CoV and MERS-CoV infections, which could thus also occur in SARS-CoV-2 infection …

Immune amplification of disease can theoretically occur in two ways. First, non-neutralizing or sub-neutralizing amounts of antibodies may amplify SARS-CoV-2 infection in target cells.

Second, antibodies could increase inflammation and thus the severity of lung disease. An overview of these antibody-dependent effects to enhance infection and immunopathology is provided in Fig. 1 …

Currently, several SARS-CoV and MERS-CoV vaccine candidates are in preclinical or early clinical trials. Animal studies with these CoVs have shown that vaccines based on the spike (S) protein (particularly the receptor-binding domain, RBD) are highly immunogenic and protective against wild-type CoVs.

Vaccines targeting other parts of the virus, such as the nucleocapsid, without the S protein have not shown protection against CoV infection and increased lung pathology. However, immunization with some S protein-based CoV vaccines has also shown evidence of increased lung pathology after infection.

Thus, in addition to the choice of antigen target, vaccine efficacy and risk of immunopathology may depend on other factors, including the formulation of the adjuvant, age at vaccination … and route of immunization.

Figure 1: Mechanism of ADE and antibody-mediated immunopathology. Left panel: In ADE, internalization of the immune complex is mediated by activation of Fc receptors on the cell surface. Co-ligation of inhibitory receptors then leads to inhibition of antiviral responses, resulting in enhanced viral replication. Right panel: antibodies can cause immunopathology by activating the complement pathway or antibody-dependent cellular cytotoxicity (ADCC). In both pathways, excessive immune activation leads to the release of cytokines and chemokines, resulting in increased disease pathology.

Do a Risk-Benefit Analysis before you decide

Ironically, the data we now have no longer support the call for mass vaccination because the lethality of COVID-19 for people under age 60 is less than that of influenza. If you are under 40 years old, your risk of dying from COVID-19 is only 0.01%, which means you have a 99.99% chance of surviving the infection. And you could increase that chance to 99.999% if you are metabolically flexible and have adequate vitamin D.

So what are we protecting against with a COVID-19 vaccine? As mentioned earlier, the vaccines are not even intended to prevent infection, but only to reduce the severity of symptoms.

And as we see now, breakthrough infections occur in up to 1 in 100 fully vaccinated people worldwide. Considering that the so-called “vaccine protection” could also cause you to get sicker once you’re exposed to the virus, that seems like a big risk for a really questionable benefit.

To return to the starting point: Neither participants in the current COVID-19 vaccine trials nor those in line for the vaccine are being told about this risk – that they could get more severe COVID-19 disease from the vaccine once they are exposed to the virus.

Lethal Th2 Immunopathology is another Potential Risk

Finally, please refer to the discussion in this PNAS article about the risk of vaccine-induced immune boosting and dysfunction, especially for the elderly who would most need the protection that a vaccine could provide:

Since the 1960s, tests of candidate vaccines against diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) have demonstrated a paradoxical phenomenon:

Some animals or humans who received the vaccine and were later exposed to the virus became more severely ill than those who had not been vaccinated. The immune system, strengthened by vaccination, appeared to show an inadequate response to natural infection in certain cases …

This immune system feedback, known as immune enhancement, can manifest in different ways, such as antibody-dependent enhancement (ADE), a process in which a virus uses antibodies to support infection, or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes may overlap …

Some investigators believe that while ADE has received the most attention to date, it is less likely to result in a dysregulated response to COVID-19 than the other immune enhancement pathways, given what is known about the epidemiology of the virus and its behavior in the human body.

There is the potential for ADE, but the bigger issue is probably Th2 immunopathology,” says Ralph Baric, an epidemiologist and expert on coronaviruses … at the University of North Carolina at Chapel Hill.

Previous studies of SARS have found aged mice to be at particularly high risk for life-threatening Th2 immunopathology … in which a faulty T-cell response triggers allergic inflammation and malfunctioning antibodies that form immune complexes, activate the complement system, and potentially damage the airways.

Fonte

1. International Journal of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795

2. PNAS.org April 14, 2020 117 (15) 8218-8221

3. Viral Immunology 2003;16(1):69-86

4. Science Direct Neutralizing Antibody

5. Science Direct Binding Antibody

6. Twitter, The Immunologist April 9, 2020

7. PLOS Pathogens 2017 Aug; 13(8): e1006565

8. Swiss Medical Weekly April 16, 2020; 150:w20249

9. Biochemical and Biophysical Research Communications August 22, 2014; 451(2): 208-214

10. JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158

11. PLOS ONE April 2012; 7(4): e35421 (PDF)

12. PLOS ONE April 2012; 7(4): e35421 (PDF), page 11

13. medRxiv DOI:10.1101/2020.03.30.20047365 (PDF)

14. EBioMedicine 2020 May; 55: 102768

15. EBioMedicine 2020 May; 55: 102768, Introduction

16. Annals of Internal Medicine September 2, 2020 DOI: 10.7326/M20-5352

17. Bitchute, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, MD, aprox 8 minutes in (Lie No. 1: Death Risk)

18. Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125

19. Johns Hopkins September 28, 2021