There has been much talk about ADE (Antibody Dependent Enhancement) from scientific skeptics of the Covid mRNA vaccine (such as Robert Malone, Luc Montagnier, et al), and a great deal of frantic censorship of their legitimate concerns by corrupt social media (Big Tech). The article on Walensky is recent and very detailed (some of it is printed below).
They’ve also been demonized and their careers ruined by snarky corrupt ‘fact-checkers’ and pundits who are paid by Big Pharma (e.g., Politifact). This only makes me believe the skeptics more, as it appears their critics have something to hide. The critics of the skeptics “doth protest too much.”
Recently, a rather conceited fellow online assured me that there’s not one shred of evidence that ADE has occurred as a result of the Covid vaccines.
Fortunately, medical journalist Sharyl Attkinsson, who looks into these things, has reported a study that seems to confirm the vaccine skeptic’s claims. Here is her article:
- Antibody Dependent Enhancement (ADE) can make vaccinated people more susceptible to serious infection from the virus
- “ADE may be a concern” for those who have been vaccinated for Covid-19
- With ADE, after people get vaccinated for an initial virus, infection by a subsequent variant or strain of the virus can result in “increased viral replication and more severe disease, leading to major safety risks”
- ADE can also “occur when neutralizing antibodies (which bind the virus and stop it from causing infection) are present at low enough levels that they don’t protect against infection. Instead, they can form immune complexes with viral particles, which in turn leads to worse illness”
- This concern was initially described by some scientists who were subsequently banned from media platforms that incorrectly claimed the scientists were disseminating disinformation
And here is the study she refers to:
I am copying the whole thing here in case they take it down later. Anything it’s possible these days.
Infection-enhancing anti-SARS-CoV-2 antibodies recognize both the original Wuhan/D614G strain and Delta variants. A potential risk for mass vaccination?
- Authors: Nouara Yahi, Henri Chahinian, Jacques Fantini
- Published:August 09, 2021DOI:https://doi.org/10.1016/j.jinf.2021.08.010
- •Infection-enhancing antibodies have been detected in symptomatic Covid-19.
- •Antibody dependent enhancement (ADE) is a potential concern for vaccines.
- •Enhancing antibodies recognize both the Wuhan strain and delta variants.
- •ADE of delta variants is a potential risk for current vaccines.
- •Vaccine formulations lacking ADE epitope are suggested.
Antibody dependent enhancement (ADE) of infection is a safety concern for vaccine strategies. In a recent publication, Li et al. (Cell 184 :4203–4219, 2021) have reported that infection-enhancing antibodies directed against the N-terminal domain (NTD) of the SARS-CoV-2 spike protein facilitate virus infection in vitro, but not in vivo. However, this study was performed with the original Wuhan/D614G strain. Since the Covid-19 pandemic is now dominated with Delta variants, we analyzed the interaction of facilitating antibodies with the NTD of these variants. Using molecular modeling approaches, we show that enhancing antibodies have a higher affinity for Delta variants than for Wuhan/D614G NTDs. We show that enhancing antibodies reinforce the binding of the spike trimer to the host cell membrane by clamping the NTD to lipid raft microdomains. This stabilizing mechanism may facilitate the conformational change that induces the demasking of the receptor binding domain. As the NTD is also targeted by neutralizing antibodies, our data suggest that the balance between neutralizing and facilitating antibodies in vaccinated individuals is in favor of neutralization for the original Wuhan/D614G strain. However, in the case of the Delta variant, neutralizing antibodies have a decreased affinity for the spike protein, whereas facilitating antibodies display a strikingly increased affinity. Thus, ADE may be a concern for people receiving vaccines based on the original Wuhan strain spike sequence (either mRNA or viral vectors). Under these circumstances, second generation vaccines with spike protein formulations lacking structurally-conserved ADE-related epitopes should be considered.The aim of the present study was to evaluate the recognition of SARS-CoV-2 Delta variants by infection enhancing antibodies directed against the NTD. The antibody studied is 1052 (pdb file #7LAB) which has been isolated from a symptomatic Covid-19 patient1. Molecular modeling simulations were performed as previously described2. Two currently circulating Delta variants were investigated, with the following mutational patterns in the NTD :
- – G142D/E154K (B.1.617.1)
- – T19R/E156G/del157/del158/A222V (B.1.617.2)
Each mutational pattern was introduced in the original Wuhan/D614G strain, submitted to energy minimization, and then tested for antibody binding. The energy of interaction (ΔG) of the reference pdb file #7LAB (Wuhan/D614G strain) in the NTD region was estimated to −229 kJ/mol−1. In the case of Delta variants, the energy of interaction was raised to −272 kJ.mol−1 (B.1.617.1) and −246 kJ.mol−1 (B.1.617.2). Thus, these infection enhancing antibodies not only still recognize Delta variants but even display a higher affinity for those variants than for the original SARS-CoV-2 strain.The global structure of the trimeric spike of the B.1.617.1 variant in the cell-facing view is shown in Fig. 1A. As expected, the facilitating antibody bound to the NTD (in green) is located behind the contact surface so that it does not interfere with virus-cell attachment. Indeed, a preformed antibody-NTD complex could perfectly bind to the host cell membrane. The interaction between the NTD and a lipid raft is shown in Fig. 1B, and a whole raft-spike-antibody complex in Fig. 1C. Interestingly, a small part of the antibody was found to interact with the lipid raft, as further illustrated in Figs. 1D-E. More precisely, two distinct loops of the heavy chain of the antibody encompassing amino acid residues 28–31 and 72–74, stabilize the complex through a direct interaction with the edge of the raft (Fig. 1F). Overall, the energy of interaction of the NTD-raft complex was raised from −399 kJ.mol−1 in absence of the antibody to −457 kJ.mol−1 with the antibody. By clamping the NTD and the lipid raft, the antibody reinforces the attachment of the spike protein to the cell surface and thus facilitates the conformational change of the RBD which is the next step of the virus infection process2.
This notion of a dual NTD-raft recognition by an infection enhancing antibody may represent a new type of ADE that could be operative with other viruses. Incidentally, our data provide a mechanistic explanation of the FcR-independent enhancement of infection induced by anti-NTD antibodies1. The model we propose, which links for the first time lipid rafts to ADE of SARS-CoV-2, is in line with previous data showing that intact lipid rafts are required for ADE of dengue virus infection3.Neutralizing antibodies directed against the NTD have also been detected in Covid-19 patients4, 5. The 4A8 antibody is a major representant of such antibodies5. The epitope recognized by this antibody on the flat NTD surface is dramatically affected in the NTD of Delta variants2, suggesting a significant loss of activity in vaccinated people exposed to Delta variants. More generally, it can be reasonably assumed that the balance between neutralizing and facilitating antibodies may greatly differ according to the virus strain (Fig. 2).
Current Covid-19 vaccines (either mRNA or viral vectors) are based on the original Wuhan spike sequence. Inasmuch as neutralizing antibodies overwhelm facilitating antibodies, ADE is not a concern. However, the emergence of SARS-CoV-2 variants may tip the scales in favor of infection enhancement. Our structural and modeling data suggest that it might be indeed the case for Delta variants.In conclusion, ADE may occur in people receiving vaccines based on the original Wuhan strain spike sequence (either mRNA or viral vectors) and then exposed to a Delta variant. Although this potential risk has been cleverly anticipated before the massive use of Covid-19 vaccines6, the ability of SARS-CoV-2 antibodies to mediate infection enhancement in vivo has never been formally demonstrated. However, although the results obtained so far have been rather reassuring1, to the best of our knowledge ADE of Delta variants has not been specifically assessed. Since our data indicate that Delta variants are especially well recognized by infection enhancing antibodies targeting the NTD, the possibility of ADE should be further investigated as it may represent a potential risk for mass vaccination during the current Delta variant pandemic. In this respect, second generation vaccines7 with spike protein formulations lacking structurally-conserved ADE-related epitopes should be considered.
- Li D.
- et al.
- Fantini J.
- Yahi N.
- Azzaz F.
- Chahinian H.
- Puerta-Guardo H.
- Mosso C.
- Medina F.
- Liprandi F.
- Ludert J.E.
- del Angel R.M.
- Chi X.
- et al.
- Liu L.
- et al.
- Iwasaki A.
- Yang Y.
- Fantini J.
- Chahinian H.
- Yahi N.
Director of CDC, Rochelle Walensky Warns of ADE, Antibody Dependent Enhancement From Israel Data
According to Robert Malone, MD inventor of the mRNA vaccine technology, a dreaded adverse side effect of COVID-19 vaccines is ADE, Antibody Dependent Enhancement which has been described in animal studies.(29)(31) This is the interaction of the immune system with the virus resulting in death of most of the vaccinated animals upon re-exposure to the virus. Obviously, this is not a good thing. (16-17)
ADE Explained: Two Types of Antibodies
In this scenario, there are two types of antibodies in the experimental animals. The first type is the neutralizing antibodies and the second type is the enhancing antibodies. The neutralizing antibodies are preferred since they “neutralize” or completely eliminate the virus from the body. The enhancing antibodies are the problem since they “enhance” entry of the virus into cells, enhancing viral replication and severity of the disease. Enhancing antibodies do exactly the opposite of the intended effect of the vaccine. Instead of protecting the animal, the vaccine makes the viral disease worse and kills the animal.(1-15)
Previous Failed Human Vaccine Trials
Previous human vaccines against RSV and Dengue virus resulted in failed vaccine trials because of ADE, Antibody Dependent Enhancement. In the Philippines, failure of the Dengue vaccine program led to criminal charges for researchers. 830,000 children were given the “Dengvaxia”, Dengue virus vaccine, before the program was suspended in 2017. (11-13) Dr Wen Shi Lee writes in Nature Microbiology (2020):
Previous respiratory syncytial virus and dengue virus vaccine studies revealed human clinical safety risks related to ADE, resulting in failed vaccine trials. (3) Endquote Dr. Lee
So far, with the mRNA COVID 19 vaccine, we have not seen this ADE to any appreciable degree in the US. However, early data from Israel suggests ADE is starting to appear in the vaccinated population, those who received their vaccination the earliest.
What is the significance of receiving your vaccine the earliest ? Pfizer is now recommending a third booster shot after 6 months, admitting the vaccine induced antibody protection wanes after 6 months or so. (14-15) In Australia, Dr Kerry Chant is bluntly stating everyone will need to get a booster vaccine every 6 months “forever”. This is an obvious admission of vaccine failure. Here is Zero Hedge quoting Dr Kerry Chant, the Australian Health Minister:
“Australian health chief Dr. Kerry Chant says that COVID will be with us “forever” and people will have to “get used to” taking endless booster vaccines.” end quote
Antibodies Wane After 6 Months
As antibodies wane, the patient is now at risk for viral infection after vaccination as we have been seeing with “break through” cases. This is the predicted scenario for ADE, and prompted Pfizer to recommend a third booster shot to avoid catastrophic ADE, as was seen with the Dengue virus in the Philippines.(1-15)