Multiple studies: COVID-19 vaccine can destroy your immune system (II)

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ADE in Dengue infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly paper published in April 2020: “The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent damage may involve the so-called antibody-dependent enhancement (ADE).

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

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

There 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 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 different from the first infection.

Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the primary infection, the longer the delay to symptomatic secondary infection (…).”

The paper goes on to detail results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue among vaccinated children under the age of 9 was greater than the rate among controls. The explanation for this appears to be that the vaccine mimicked a primary 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 analysis of efficacy trials, using an anti-nonstructural protein 1 immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-type 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 among seronegative persons.

Based on this, a Strategic Advisor Group of Experts convened by World Health Organization (WHO) concluded that only Dengue seropositive persons should be 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-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 after vaccination, and only those who have already recovered from a bout of COVID-19 would be protected against severe illness by the vaccine.

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

The Swiss Medical Weekly paper 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 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 immunophathology once 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, “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 (programed cell death – red. note).

Results from infectivity assays indicate 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 suggest that antibodies against SARS-CoV spike proteins may trigger ADE effects. The data raise new questions regarding a potential SARS-CoV vaccine (…).”

A study that ties into this was published in the journal JCI Insight (Journal of Clinical Investigation Insight) in 2019. Here, 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 developed acute diffuse alveolar damage, likely by “skewing the inflammation-resolving response.”

SARS vaccine worsens 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,” demonstrates what many researchers now fear, namely that COVID-19 vaccines may end up making people more prone to severe SARS-CoV-2 infection. The paper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunophathology once challenged with the SARS virus. As noted by the authors: “Inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2 (lymphocyte T helper 2 – red. note) –type immunopathologic in lungs after challenge.

As indicated, two reports attributed the immunopathology to presence of the N 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-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four 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 preparation that does not induce this result in mice, ferrets and nonhuman primates has not been reported.

This combined experience provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines have been conducted and reported to induce antibody responses and to be ‘safe.’ However, the evidence for safety is for a short period of observation.

The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional safety 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’s evidence showing the elderly – who are most vulnerable to severe COVID-19 – are also the most vulnerable to ADE. Preliminary research findings 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 concern

Another paper worth mentioning is the May 2020 minireview “Impact of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development.” As in many other papers, the authors point out that: “While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical safety 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-2 infection. (…)

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

Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. (…)

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 spike (S) 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 have 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 route of immunization.”

Do a risk-benefit analysis before making up your conscience

Ironically, the data now exist 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. If you’re under the age of 40, your risk of dying from COVID-19 is just 0.01%, meaning you have a 99.99% chance 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 against with a COVID-19 vaccine? As mentioned, the vaccines aren’t even designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you’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-19 vaccine trials are not being 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 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 most: “Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) have shown a paradoxical phenomenon: Some animals or people who received the vaccine and were later exposed to the virus developed more severe 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 immune backfiring, or so-called immune enhancement, may manifest in different ways such as antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes might overlap …

Some researchers argue that although ADE has received the most attention to date, it 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 human body.”

‘There is the potential for ADE, but 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 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.”

yogaesoteric,
May 31, 2021