How Do You Know the Disease of Hiv Has Progressed to Aids

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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 than severe illness if they're exposed to the virus.

The report,¹ "Informed Consent Disclosure to Vaccine Trial Subjects of Take a chance of COVID-19 Vaccine Worsening Clinical Illness," published in the International Journal of Clinical Practise, October 28, 2020, points out that "COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated."

"Vaccines for SARS, MERS and RSV have never been canonical, and the data generated in the development and testing of these vaccines suggest a serious mechanistic concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral fasten to elicit neutralizing antibodies), be they equanimous of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE)," the paper states.

"This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 vaccine trials that adequate patient comprehension of this run a risk is unlikely to occur, obviating truly informed consent by subjects in these trials.

The specific and significant COVID-19 adventure of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well as those existence recruited for the trials and time to come patients after vaccine approval, in social club to come across the medical ethics standard of patient comprehension for informed consent."

What Is Antibody-Dependent Enhancement?

Equally noted past the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for severe acute 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 trend to trigger antibody-dependent enhancement.

What exactly does that mean? In a nutshell, it means that rather than heighten your immunity confronting the infection, the vaccine actually enhances the virus' ability to enter and infect your cells, resulting in more severe disease than had y'all not been vaccinated. ²

This is the exact opposite of what a vaccine is supposed to do, and a significant problem that has been pointed out from the very commencement of this push for a COVID-xix vaccine. The 2003 review newspaper "Antibiotic-Dependent Enhancement of Virus Infection and Disease" explains it this style:^three

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

The ADE of virus infection is a miracle in which virus-specific antibodies raise 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 as preferential replication in macrophages, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a peachy concern to disease command past vaccination."

Previous Coronavirus Vaccine Efforts Have All Failed

In my May 2020 interview to a higher place with Robert Kennedy Jr., he summarized the history of coronavirus vaccine evolution, which began in 2002, following iii consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had most 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 full interview, Kennedy explains what happened next. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, in one case they were challenged with the wild virus, they all became severely sick and died.

The same affair happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory illness that is very similar to that caused by coronaviruses. At that time, they had decided to skip creature trials and become direct to human being trials.

"They tested it on I remember about 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 ill. Two of them died. They abased the vaccine. It was a big embarrassment to FDA and NIH."

Neutralizing Versus Binding Antibodies

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

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

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known every bit "paradoxical immune enhancement." Another way to look at this is your immune system is actually backfiring and not functioning to protect you but really making y'all worse.

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to make the SARS-CoV-two fasten protein (S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the start stage of the two-stage procedure viruses use to proceeds entry into cells.

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

Without Neutralizing Antibodies, Expect More Severe Illness

In an Apr 2020 Twitter thread,^vi The Immunologist noted: "While developing vaccines ... and considering immunity passports, we must offset 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 about ADE.

The first 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 bailiwick against reinfection, as is typically the case with many viral illnesses. (Meaning, once you recover from a viral infection, say measles, you lot're immune and won't contract the affliction again.)

To determine how MERS affects the immune 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 event, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill again, and more severely so.

"In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers," the authors noted. Interestingly, neutralizing antibodies were elicited during this second infection, preventing the animals from being infected a 3rd time. According to the authors:

"Our information from the rabbit model suggests that people exposed to MERS-CoV who neglect to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may exist at hazard for severe lung disease on re-exposure to MERS-CoV."

In other words, if the vaccine does not effect in a robust response in neutralizing antibodies, you might be at risk for more severe lung disease if you lot're infected with the virus.

And here's an important point: COVID-nineteen vaccines are Non designed to preclude infection. As detailed in "How COVID-xix Vaccine Trials Are Rigged," a "successful" vaccine but needs to reduce the severity of the symptoms. They're non even looking at reducing infection, hospitalization or death rates.

ADE in Dengue Infections

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

"The pathogenesis of COVID-19 is currently believed to keep via both direct cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral jail cell entry and subsequent damage 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 miracle is of enormous relevance not only for the understanding of viral pathogenesis, but likewise for developing antiviral strategies, notably vaccines ...

At that place are four 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 only up to 2 years.

In Dengue fever, reinfection with a unlike serotype runs a more severe course when the protective antibody titer wanes. Here, non-neutralizing antibodies take over neutralizing ones, demark 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 different from the first 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 item results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization charge per unit for Dengue amid vaccinated children under the age of 9 was greater than the rate among controls. The explanation for this appears to exist that the vaccine mimicked a primary infection, and equally that immunity waned, the children became susceptible to ADE when they encountered the virus a 2d time. The author explains:

"A mail service hoc analysis of efficacy trials, using an anti-nonstructural protein one immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-type infection from those post-obit 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 run a risk of astringent clinical outcome was increased among seronegative persons.

Based on this, a Strategic Advisor Grouping of Experts convened by Globe Health Arrangement (WHO) concluded that just Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination."

ADE in Coronavirus Infections

This could end upwardly being important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, so anyone who has not tested positive for SARS-CoV-2 might really be at increased risk for severe COVID-xix after vaccination, and only those who have already recovered from a bout of COVID-nineteen would be protected against severe disease by the vaccine.

To be clear, we do not know whether that is the case or not, only these are important areas of inquiry and the current vaccine trials volition simply not exist able to answer this important question.

The Swiss Medical Weekly paper ⁹ also reviews the evidence of ADE in coronavirus infections, citing research showing inoculating cats against the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the affliction when challenged with the same FIPV serotype equally that in the vaccine.

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

The paper also cites enquiry showing "Antibodies elicited by a SARS-CoV vaccine enhanced infection of B jail cell lines in spite of protective responses in the hamster model." Some other paper,^ten "Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Confronting Fasten 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 point that SARS-CoV ADE is primarily mediated past diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. We likewise generated monoclonal antibodies confronting 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 effects. The data raise new questions regarding a potential SARS-CoV vaccine ..."

A written report^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 poly peptide ended upwards with more than 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 harm, likely by "skewing the inflammation-resolving response."

SARS Vaccine Worsens Infection After Challenge With SARS-CoV

An interesting 2012 newspaper ¹² with the telling title, "Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Claiming with the SARS Virus," demonstrates what many researchers now fear, namely that COVID-19 vaccines may end upwardly making people more decumbent to severe SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a diverseness of SARS vaccines resulted in pulmonary immunopathology in one case 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-blazon immunopathologic in lungs after claiming.

As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; notwithstanding, we found the same immunopathologic reaction in animals given S protein vaccine only, although information technology appeared to be of bottom 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 different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine training that does not induce this upshot 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 'safety.' Notwithstanding, the evidence for safety is for a curt period of observation.

The business organisation arising from the nowadays 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 relate to effectiveness and safe confronting 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 tiptop of all of these concerns, there'southward evidence showing the elderly — who are most vulnerable to severe COVID-19 — are also the almost vulnerable to ADE. Preliminary research findings^xiv posted on the preprint server medRxiv at the finish of March 2020 reported that middle-aged and elderly COVID-xix patients take far college levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.

Allowed Enhancement Is a Serious Concern

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

"While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-ii are promising, they both pose a common theoretical safety concern. Experimental studies have suggested the possibility of immune-enhanced illness 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 2 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 affliction. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. one ...

Currently, in that location are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Beast studies on these CoVs have shown that the spike (Due south) protein-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 as the nucleocapsid, without the S protein, have shown no protection against CoV infection and increased lung pathology. However, immunization with some S protein based CoV vaccines take as well displayed signs of enhanced lung pathology following challenge.

Hence, as well the choice of antigen target, vaccine efficacy and risk of immunopathology may be dependent on other ancillary factors, including adjuvant conception, age at vaccination ... and road of immunization."

© articles.mercola.com
Figure 1: Machinery of ADE and antibody mediated immunopathology. Left panel: For ADE, immune circuitous internalization is mediated by the appointment of activating Fc receptors on the jail cell surface. Co-ligation of inhibitory receptors and so results in the inhibition of antiviral responses which leads to increased viral replication. Right console: 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.

Do a Risk-Benefit Assay Earlier Making Upward Your Mind

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

Ironically, the data ^17,18,xix we now accept 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 age of 40, your risk of dying from COVID-19 is just 0.01%, meaning y'all have a 99.99% chance of surviving the infection. And y'all 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-xix vaccine? Every bit mentioned, the vaccines aren't even designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you lot 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 existence told of this risk — that by getting the vaccine they may end 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 take chances of vaccine-induced immune enhancement and dysfunction, peculiarly for the elderly, the very people who would need the protection a vaccine might offer the most:²¹

"Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe astute respiratory syndrome (SARS) have shown a paradoxical phenomenon:

Some animals or people who received the vaccine and were later exposed to the virus developed more astringent disease than those who had not been vaccinated. The vaccine-primed immune system, 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 assist infection; or prison 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 attending to appointment, information technology is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its behavior in the homo body.

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

In previous studies of SARS, aged mice were found to have particularly loftier risks of life-threatening Th2 immunopathology ... in which a faulty T jail cell response triggers allergic inflammation, and poorly functional antibodies that class immune complexes, activating the complement system and potentially damaging the airways."

Sources and References

• 1 International Journal of Clinical Do, Oct 28, 2020 DOI: 10.111/ijcp.13795
• 2, 21 PNAS.org Apr 14, 2020 117 (fifteen) 8218-8221
• 3 Viral Immunology 2003;xvi(1):69-86
• 4 Science Directly Neutralizing Antibody
• 5 Science Direct Bounden Antibody
• 6 Twitter, The Immunologist April ix, 2020
• 7 PLOS Pathogens 2017 Aug; 13(8): e1006565
• 8, nine Swiss Medical Weekly April xvi, 2020; 150:w20249
• 10 Biochemical and Biophysical Enquiry Communications August 22, 2014; 451(two): 208-214
• 11 JCI Insight February 21, 2019 DOI: x.1172/jci.insight.123158
• 12 PLOS ONE April 2012; 7(four): e35421 (PDF)
• 13 PLOS Ane April 2012; seven(4): e35421 (PDF), folio xi
• fourteen medRxiv DOI:x.1101/2020.03.xxx.20047365 (PDF)
• fifteen EBioMedicine 2020 May; 55: 102768
• 16 EBioMedicine 2020 May; 55: 102768, Introduction
• 17, 20 Annals of Internal Medicine September 2, 2020 DOI: 10.7326/M20-5352
• 18 YouTube, SARS-CoV-2 and the rise of medical technocracy, Lee Merritt, Doc, aprox eight minutes in (Prevarication No. 1: Expiry Risk)
• 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