Shahid Masood at Internal Medicine & Family Practice

© Image by Gerd Altmann from Pixabay

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

The study,¹ "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-xix 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 severe affliction than if they were not vaccinated."

"Vaccines for SARS, MERS and RSV have never been approved, and the information generated in the development and testing of these vaccines suggest a serious mechanistic business organisation: that vaccines designed empirically using the traditional arroyo (consisting of the unmodified or minimally modified coronavirus viral spike to arm-twist neutralizing antibodies), exist they equanimous of protein, viral vector, Dna or RNA and irrespective of delivery method, may worsen COVID-xix affliction via antibody-dependent enhancement (ADE)," the paper states.

"This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-nineteen vaccine trials that adequate patient comprehension of this risk is unlikely to occur, obviating truly informed consent past subjects in these trials.

The specific and pregnant COVID-19 risk of ADE should have been and should be prominently and independently disclosed to enquiry subjects currently in vaccine trials, every bit well as those beingness recruited for the trials and future patients after vaccine approval, in order 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 severe astute respiratory syndrome coronavirus (SARS-CoV), Centre East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — take revealed a serious business concern: The vaccines have a tendency to trigger antibiotic-dependent enhancement.

What exactly does that hateful? In a nutshell, it means that rather than heighten your amnesty against the infection, the vaccine actually enhances the virus' ability to enter and infect your cells, resulting in more astringent disease than had you not been vaccinated. ⁱⁱ

This is the exact contrary of what a vaccine is supposed to do, and a meaning problem that has been pointed out from the very start of this push for a COVID-19 vaccine. The 2003 review paper "Antibody-Dependent Enhancement of Virus Infection and Affliction" explains it this mode:³

"In full general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of means. Notwithstanding, in some instances, the presence of specific antibodies tin be beneficial to the virus. This action is known as antibiotic-dependent enhancement (ADE) of virus infection.

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

This miracle 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 as preferential replication in macrophages, ability to establish persistence, and antigenic multifariousness. For some viruses, ADE of infection has become a peachy concern to illness command by vaccination."

Previous Coronavirus Vaccine Efforts Accept All Failed

In my May 2020 interview to a higher place 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 four all-time vaccine candidates were so given to ferrets, which are the closest analogue to human being 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 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 matter happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory disease that is very similar to that caused by coronaviruses. At that time, they had decided to skip animal trials and get straight to human trials.

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

Neutralizing Versus Binding Antibodies

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

• Neutralizing antibodies,⁴ also referred to as 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, bounden antibodies trigger an abnormal immune response known as "paradoxical immune enhancement." Another manner to await at this is your immune system is really backfiring and not functioning to protect you only really making you worse.

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

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

Without Neutralizing Antibodies, Wait More Severe Disease

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

The beginning 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 subject against reinfection, as is typically the case with many viral illnesses. (Pregnant, once you lot recover from a viral infection, say measles, you lot're allowed and won't contract the illness over again.)

To make up one's mind how MERS affects the allowed system, the researchers infected white rabbits with the virus. The rabbits got ill and developed antibodies, but those antibodies were not the neutralizing kind, meaning the kind of antibodies that block infection. As a result, they were non protected from reinfection, and when exposed to MERS for a second time, they became sick over again, and more severely then.

"In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increment 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. Co-ordinate 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 have waned, may exist at hazard 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 lot might be at risk for more severe lung disease if you're infected with the virus.

And hither'southward an important indicate: COVID-19 vaccines are NOT designed to preclude 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 not even looking at reducing infection, hospitalization or decease rates.

ADE in Dengue Infections

The Dengue virus is too known to crusade ADE. Equally explained in a Swiss Medical Weekly paper published in April 2020:^eight

"The pathogenesis of COVID-19 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 and so-called antibody-dependent enhancement (ADE).

ADE is a very well-known pour 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, only besides for developing antiviral strategies, notably vaccines ...

There are four serotypes of Dengue virus, all eliciting protective amnesty. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against unlike serotypes are curt-lived and may last only up to ii years.

In Dengue fever, reinfection with a different serotype runs a more severe course 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 unlike from the offset infection.

Cantankerous-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 delay to symptomatic secondary infection ..."

The paper goes on to detail results from follow-upwardly investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue amidst vaccinated children nether the age of nine was greater than the rate amidst controls. The explanation for this appears to be that the vaccine mimicked a chief infection, and equally that immunity waned, the children became susceptible to ADE when they encountered the virus a second time. The author explains:

"A post hoc assay of efficacy trials, using an anti-nonstructural protein 1 immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by 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 amidst seronegative persons.

Based on this, a Strategic Advisor Group of Experts convened by Earth 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 terminate up beingness of import for the COVID-xix vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, then anyone who has non tested positive for SARS-CoV-2 might actually be at increased risk for severe COVID-19 after vaccination, and simply those who have already recovered from a tour of COVID-19 would exist protected against astringent disease by the vaccine.

To be clear, we practise non know whether that is the case or not, but these are important areas of inquiry and the current vaccine trials volition but not be able to respond this important question.

The Swiss Medical Weekly newspaper ⁹ also reviews the testify of ADE in coronavirus infections, citing research showing inoculating cats confronting 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 variety of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus.

The newspaper also cites research showing "Antibodies elicited by a SARS-CoV vaccine enhanced infection of B jail cell lines in spite of protective responses in the hamster model." Another newspaper,¹⁰ "Antibody-Dependent SARS Coronavirus Infection Is Mediated past Antibodies Against Spike Proteins," published in 2014, constitute 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 bespeak that SARS-CoV ADE is primarily mediated by diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. We also generated monoclonal antibodies against SARS-CoV spike 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 raise new questions regarding a potential SARS-CoV vaccine ..."

A study^eleven that ties into this was published in the journal JCI Insight in 2019. Hither, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike protein ended 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 harm, likely by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Later on Claiming With SARS-CoV

An interesting 2012 paper ¹² with the telling title, "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 upwards 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. As noted past the authors: ¹³

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.

Equally indicated, ii reports attributed the immunopathology to presence of the N protein in the vaccine; nonetheless, nosotros found the same immunopathologic reaction in animals given S poly peptide vaccine only, although it appeared to be of lesser intensity.

Thus, a Th2-blazon immunopathologic reaction on challenge of vaccinated animals has occurred in 3 of four beast models (non in hamsters) including 2 unlike inbred mouse strains with four 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 not been reported.

This combined experience provides business 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.' Still, the show for rubber is for a short period of observation.

The concern arising from the present written report is for an immunopathologic reaction occurring amid vaccinated individuals on exposure to infectious SARS-CoV, the footing for developing a vaccine for SARS. Additional safety concerns chronicle to effectiveness and safety against antigenic variants of SARS-CoV and for prophylactic of vaccinated persons exposed to other coronaviruses, particularly those of the type ii group."

The Elderly Are Most Vulnerable to ADE

On top of all of these concerns, there's evidence showing the elderly — who are almost vulnerable to severe COVID-19 — are also the most vulnerable to ADE. Preliminary research findings¹⁴ posted on the preprint server medRxiv at the end of March 2020 reported that middle-aged and elderly COVID-19 patients have far higher levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.

Immune Enhancement Is a Serious Business

Another newspaper worth mentioning is the May 2020 mini review¹⁵ "Impact of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development." As in many other papers, the authors bespeak out that:^xvi

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical condom concern. Experimental studies have suggested the possibility of immune-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-two infection ...

Immune enhancement of disease can theoretically occur in two means. Firstly, non-neutralizing or sub-neutralizing levels of antibodies tin enhance SARS-CoV-2 infection into target cells.

Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. i ...

Currently, at that place are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animal studies on these CoVs take shown that the spike (Southward) protein-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective against wild-type CoV claiming.

Vaccines that target other parts of the virus, such as the nucleocapsid, without the S poly peptide, accept shown no protection against CoV infection and increased lung pathology. Withal, immunization with some South protein based CoV vaccines have as well displayed signs of enhanced lung pathology post-obit challenge.

Hence, besides the selection of antigen target, vaccine efficacy and gamble of immunopathology may be dependent on other ancillary factors, including adjuvant formulation, age at vaccination ... and route of immunization."

© manufactures.mercola.com
Effigy 1: Machinery of ADE and antibody mediated immunopathology. Left console: For ADE, allowed complex internalization is mediated by the engagement of activating Fc receptors on the cell surface. Co-ligation of inhibitory receptors and 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 antibody-dependent cellular cytotoxicity (ADCC). For both pathways, excessive immune activation results in the release of cytokines and chemokines, leading to enhanced disease pathology.

Exercise a Take a chance-Do good Analysis Before Making Up Your Heed

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end up being, they'll be released to the public in relatively short order. Virtually predict ane or more vaccines will be set up sometime in 2021.

Ironically, the data ^{17,eighteen,19} we now take no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60. ²⁰ If you lot're under the age of 40, your run a risk of dying from COVID-xix is just 0.01%, meaning you have a 99.99% adventure of surviving the infection. And you could improve that to 99.999% if you're metabolically flexible and vitamin D replete.

So, really, what are nosotros protecting against with a COVID-19 vaccine? Equally mentioned, the vaccines aren't even designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially brand yous sicker once you lot're exposed to the virus. That seems similar 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 stop upwardly with more astringent COVID-nineteen once they're infected with the virus.

Lethal Th2 Immunopathology Is Some other Potential Adventure

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

Some animals or people who received the vaccine and were afterward exposed to the virus developed more astringent disease 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 allowed backfiring, or then-called immune enhancement, may manifest in different ways such as antibiotic-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 by Th2 immunopathology. In some cases, the enhancement processes might overlap ...

Some researchers contend that although ADE has received the most attending to date, it is less probable than the other immune enhancement pathways to crusade a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its behavior in the human body.

'There is the potential for ADE, only the bigger problem is probably Th2 immunopathology,' says Ralph Baric, an epidemiologist and expert in coronaviruses ... at the University of North Carolina at Chapel Hill.

In previous studies of SARS, aged mice were constitute to take particularly high risks of life-threatening Th2 immunopathology ... in which a faulty T prison cell response triggers allergic inflammation, and poorly functional antibodies that course immune complexes, activating the complement system and potentially dissentious the airways."

Sources and References

• i International Journal of Clinical Exercise, Oct 28, 2020 DOI: 10.111/ijcp.13795
• 2, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
• three Viral Immunology 2003;sixteen(1):69-86
• 4 Science Straight Neutralizing Antibody
• 5 Scientific discipline Straight Binding Antibody
• half dozen Twitter, The Immunologist April nine, 2020
• 7 PLOS Pathogens 2017 Aug; 13(viii): e1006565
• eight, 9 Swiss Medical Weekly Apr 16, 2020; 150:w20249
• 10 Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(2): 208-214
• eleven JCI Insight February 21, 2019 DOI: 10.1172/jci.insight.123158
• 12 PLOS ONE April 2012; 7(4): e35421 (PDF)
• 13 PLOS ONE Apr 2012; vii(iv): e35421 (PDF), folio eleven
• 14 medRxiv DOI:10.1101/2020.03.thirty.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-2 and the rise of medical technocracy, Lee Merritt, MD, aprox viii minutes in (Lie No. 1: Decease Run a risk)
• 19 Technical Report June 2020 DOI: 10.13140/RG.2.24350.77125

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Source: https://www.sott.net/article/445095-How-COVID-19-vaccine-can-destroy-your-immune-system