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Co-ordinate 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 brand them susceptible to more severe disease if they're exposed to the virus.

The study,ⁱ "Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-nineteen Vaccine Worsening Clinical Disease," published in the International Periodical of Clinical Practice, October 28, 2020, points out that "COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe affliction 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 concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), be they composed of protein, viral vector, Deoxyribonucleic acid or RNA and irrespective of delivery method, may worsen COVID-xix disease via antibiotic-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 risk is unlikely to occur, obviating truly informed consent by subjects in these trials.

The specific and significant COVID-xix run a risk of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, also as those being recruited for the trials and hereafter patients later vaccine approval, in order to come across the medical ethics standard of patient comprehension for informed consent."

What Is Antibody-Dependent Enhancement?

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

What exactly does that mean? In a nutshell, it ways that rather than enhance your immunity against the infection, the vaccine really enhances the virus' ability to enter and infect your cells, resulting in more than severe illness than had you not been vaccinated. ⁱⁱ

This is the verbal opposite of what a vaccine is supposed to practice, and a significant problem that has been pointed out from the very starting time of this push for a COVID-19 vaccine. The 2003 review newspaper "Antibiotic-Dependent Enhancement of Virus Infection and Disease" explains it this style: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. Yet, in some instances, the presence of specific antibodies can be benign to the virus. This activity is known every bit 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 mutual features such every bit preferential replication in macrophages, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a dandy business organisation to illness control by vaccination."

Previous Coronavirus Vaccine Efforts Accept 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 3 consecutive SARS outbreaks. Past 2012, Chinese, American and European scientists were working on SARS vaccine development, and had near 30 promising candidates.

Of those, the four best vaccine candidates were then 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 adjacent. 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 fourth dimension, they had decided to skip animate being trials and go directly to human trials.

"They tested it on I think near 35 children, and the same thing 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. Information technology was a big embarrassment to FDA and NIH."

Neutralizing Versus Binding Antibodies

Coronaviruses produce not simply i simply ii different types of antibodies:

• Neutralizing antibodies,⁴ likewise referred to equally immunoglobulin Yard (IgG) antibodies, that fight the infection
• Bounden antibodies⁵ (also known equally non-neutralizing antibodies) that cannot preclude viral infection

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

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to brand the SARS-CoV-2 fasten protein (Due south poly peptide). The spike protein, which is what attaches to the ACE2 receptor of the prison cell, is the offset phase of the two-stage procedure viruses use to gain entry into cells.

The thought is that by creating the SARS-CoV-2 spike protein, your allowed organisation will embark product of antibodies, without making you sick in the process. The key question is, which of the two types of antibodies are existence produced through this process?

Without Neutralizing Antibodies, Expect More than Severe Illness

In an April 2020 Twitter thread,^vi The Immunologist noted: "While developing vaccines ... and because immunity passports, we must get-go 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 nearly ADE.

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

To determine how MERS affects the immune organization, the researchers infected white rabbits with the virus. The rabbits got sick and developed antibodies, but those antibodies were non the neutralizing kind, pregnant the kind of antibodies that cake infection. As a result, they were non protected from reinfection, and when exposed to MERS for a second fourth dimension, they became sick once more, 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 2d infection, preventing the animals from being infected a tertiary time. According to the authors:

"Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibiotic response, or persons whose neutralizing antibody titers have waned, may be at risk for astringent 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 take a chance for more than astringent lung illness if you're infected with the virus.

And here's an important point: COVID-xix vaccines are NOT designed to preclude infection. As detailed in "How COVID-19 Vaccine Trials Are Rigged," a "successful" vaccine only needs to reduce the severity of the symptoms. They're non fifty-fifty looking at reducing infection, hospitalization or death rates.

ADE in Dengue Infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly newspaper published in April 2020:⁸

"The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and immune-mediated mechanisms. An boosted mechanism facilitating viral cell entry and subsequent harm may involve the 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 distension of their replication.

This phenomenon is of enormous relevance not only for the understanding of viral pathogenesis, but also for developing antiviral strategies, notably vaccines ...

There are 4 serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may last merely up to 2 years.

In Dengue fever, reinfection with a unlike serotype runs a more astringent grade 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 business relationship for ADE in persons infected with a serotype of Dengue virus that is dissimilar from the outset 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 delay to symptomatic secondary infection ..."

The newspaper goes on to detail results from follow-upwards investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue among vaccinated children nether the age of ix was greater than the rate amongst controls. The explanation for this appears to exist that the vaccine mimicked a main infection, and as 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 earlier vaccination, and that the chance of severe clinical upshot was increased among seronegative persons.

Based on this, a Strategic Advisor Group of Experts convened by World Wellness System (WHO) ended that but Dengue seropositive persons should exist vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could end up being important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-ii works like Dengue, which is besides caused by an RNA virus, so anyone who has not tested positive for SARS-CoV-2 might actually be at increased risk for severe COVID-19 later on vaccination, and only those who take already recovered from a bout of COVID-19 would be protected against severe illness by the vaccine.

To be clear, we do non know whether that is the case or not, merely these are important areas of inquiry and the current vaccine trials will just not exist able to respond this important question.

The Swiss Medical Weekly paper ^ix also reviews the prove of ADE in coronavirus infections, citing research showing inoculating cats against the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the disease when challenged with the same FIPV serotype as that in the vaccine.

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

The paper also 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 "Antibody-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 past diluted antibodies against envelope fasten proteins rather than nucleocapsid proteins. We likewise generated monoclonal antibodies against SARS-CoV fasten proteins and observed that about of them promoted SARS-CoV infection.

Combined, our results suggest that antibodies against SARS-CoV spike proteins may trigger ADE effects. The data 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 ended upwards 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 developed astute diffuse alveolar impairment, likely past "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection Afterwards Challenge With SARS-CoV

An interesting 2012 paper ¹² with the telling championship, "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus," demonstrates what many researchers at present fear, namely that COVID-19 vaccines may stop upwardly making people more than prone to severe SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunopathology once challenged with the SARS virus. As noted by 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.

As indicated, ii reports attributed the immunopathology to presence of the Due north protein in the vaccine; however, we found the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity.

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

This combined feel provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines take been conducted and reported to induce antibody responses and to be 'safe.' Yet, the show for safety is for a short menses of observation.

The business organisation arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the footing for developing a vaccine for SARS. Boosted prophylactic concerns relate to effectiveness and safety 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'south evidence showing the elderly — who are about vulnerable to severe COVID-19 — are also the nearly vulnerable to ADE. Preliminary research findings¹⁴ posted on the preprint server medRxiv at the end of March 2020 reported that centre-anile and elderly COVID-19 patients have far higher levels of anti-fasten antibodies — which, once again, increment infectivity — than younger patients.

Immune Enhancement Is a Serious Concern

Another paper worth mentioning is the May 2020 mini review¹⁵ "Touch on of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development." As in many other papers, the authors point out that:¹⁶

"While evolution of both hyperimmune globulin therapy and vaccine against SARS-CoV-ii are promising, they both pose a common theoretical safe concern. Experimental studies have suggested the possibility of allowed-enhanced disease 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, not-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 furnishings 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 (South) poly peptide-based vaccines (specifically the receptor binding 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 South protein, take shown no protection confronting CoV infection and increased lung pathology. However, immunization with some Southward protein based CoV vaccines take also displayed signs of enhanced lung pathology following challenge.

Hence, besides 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."

© articles.mercola.com
Figure 1: Mechanism of ADE and antibody mediated immunopathology. Left panel: For ADE, immune complex internalization is mediated past the engagement of activating Fc receptors on the cell surface. Co-ligation of inhibitory receptors so results in the inhibition of antiviral responses which leads to increased viral replication. Right panel: Antibodies tin 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.

Exercise a Gamble-Benefit Analysis Before Making Up Your Listen

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end upward existence, they'll be released to the public in relatively short club. Most predict one or more vaccines volition be ready sometime in 2021.

Ironically, the data ^17,18,19 we now have no longer support a mass vaccination mandate, considering the lethality of COVID-xix is lower than the flu for those under the age of sixty. ²⁰ If you're under the age of 40, your risk of dying from COVID-xix is simply 0.01%, meaning you have a 99.99% gamble 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 we protecting confronting with a COVID-19 vaccine? As mentioned, the vaccines aren't even designed to preclude infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you lot'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-nineteen vaccine trials are not beingness told of this gamble — that by getting the vaccine they may end upwards with more than severe COVID-19 once they're infected with the virus.

Lethal Th2 Immunopathology Is Some other Potential Risk

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

"Since the 1960s, tests of vaccine candidates for diseases such equally dengue, respiratory syncytial virus (RSV), and astringent 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 severe 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 so-chosen allowed enhancement, may manifest in dissimilar means such every bit 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 past Th2 immunopathology. In some cases, the enhancement processes might overlap ...

Some researchers argue that although ADE has received the most attention to date, it is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-xix, given what is known about the epidemiology of the virus and its beliefs in the human torso.

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

In previous studies of SARS, aged mice were found to have 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 system and potentially damaging the airways."

Sources and References

• 1 International Periodical of Clinical Practice, October 28, 2020 DOI: 10.111/ijcp.13795
• 2, 21 PNAS.org April 14, 2020 117 (15) 8218-8221
• 3 Viral Immunology 2003;16(1):69-86
• 4 Science Direct Neutralizing Antibody
• five Science Direct Binding Antibody
• vi Twitter, The Immunologist April 9, 2020
• 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
• 8, 9 Swiss Medical Weekly Apr xvi, 2020; 150:w20249
• 10 Biochemical and Biophysical Inquiry Communications August 22, 2014; 451(2): 208-214
• 11 JCI Insight Feb 21, 2019 DOI: ten.1172/jci.insight.123158
• 12 PLOS Ane April 2012; 7(4): e35421 (PDF)
• 13 PLOS ONE April 2012; 7(4): e35421 (PDF), page 11
• xiv 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 two, 2020 DOI: x.7326/M20-5352
• xviii YouTube, SARS-CoV-2 and the ascension of medical technocracy, Lee Merritt, MD, aprox eight minutes in (Lie No. ane: Decease Take chances)
• 19 Technical Report June 2020 DOI: ten.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