💉 COVID-19 Vaccine Side Effects And Long Haul COVID-19 Caused By Anti-idiotype Antibodies
In light of mounting COVID-19 vaccine adverse events like allergic reactions, myocarditis, thrombosis, immune thrombocytopenia, additionally long haul COVID-19 cases, and finally symptoms from COVID-19, researchers have scoured the data to find answers. Interestingly enough, the quest for answers lead researchers to the re-discovery of Network Hypothesis by the 1984 Nobel Prize winner Dr. Niels Jerne1. To summarize, the answer to what’s causing long haul COVID-19, many SARS-COV-2 vaccine side effects, and complications from natural infection, could be explained by antibodies that mimic the viruses spike protein which could cause damage for prolonged periods of time2 3. That said, all salient data will be presented in this publication. Succinctly put, you will learn 3 things:
First, you will learn a brief history of how researchers stumbled upon this potential answer to what’s causing COVID-19 vaccine induced side effects, long haul COVID-19, and pathology from natural exposure to the virus
Second, you will learn about essential details from data in new medical publications that show how vaccine side effects, long haul covid, and pathology from natural exposure to SARS-CoV-2 could be caused by anti-idiotype antibodies
Third, you will learn about realistic measures that could be taken to reduce the occurrence of COVID-19 vaccine induced side effects, long haul COVID-19, and deleterious effects of pathology from natural exposure to SARS-CoV-2
📚 To begin, some history
In order to understand the implications of the data that will be presented later in this publication, you first need some historical context regarding the creator of this potential answer to the previously stated problem. That being, the credentials and background of Dr. Neils Jerne who’s Network Hypothesis will be shared farther down.
Lets start here ➡️ Dr. Niels K. Jerne first received a baccalaureate degree in physics pre-war 1928. Following that, the plan was to study medicine. However the Second World War put a pause on his academic endeavors for sometime. After a long educational break, Niels began immunologic research at the Danish State Serum Institute in 1943. As time passed, an M.D. was achieved in 1951 through the University of Copenhagen. Fast forward to 1954, Dr. Niels spent 12 months as a research fellow at the California Institute of Technology within the Max Delbruck’s laboratory studying immunology. It wasn’t long until experience and credentials allowed the doctor to head the Biological Standards and Immunology departments at the World Health Organization between 1956-1962. Within a short period of time, Dr. Neils K Jerne then chaired the Department of Microbiology at the University of Pittsburgh in 1962 where he stayed 4 years. Next, Dr. Neils co-founded the Basil Institute of Immunology where he was a director and researched for many years. Importantly, 1974 was the inception of Dr. Neils Network Hypothesis theory that denoted how viruses and some bacteria can force hosts (humans) to generate anti-idiotypic antibodies against themselves which can create substantial damage. Now, as a culmination of academic and professional endeavors, Dr. Neils received a Nobel Prize in 1973 for 3 of his theories (including Network Hypothesis) which still serve as the foundation of modern immunology today. As a side note, please see 📸 FIG.1 below listing all Dr. Neils K. Jerne’s academic and professional achievements 👇🏻.
Onto the main point. Collectively, Dr. Neils’ lifelong work in immunology made his theory of Network Hypothesis a strong candidate for consideration as current medical researchers at UC Davis attempt to demystify why so many people experience such terrible side effects after vaccination and natural infection. Therefore, below, Network Hypothesis will be explained in bullet points and images created just for you.
🔔 SO WHAT DOES ALL OF THIS MEAN?
Succinctly put, Dr. Neils K. Jerne is a world authority on immunology and because of that, his NETWORK HYPOTHESIS is being considered as a potential mechanism for why individuals are experiencing such grueling side effects after both COVID-19 vaccination, and natural infection.
📸 FIG.1
📝 Network Hypothesis- Research on how anti-idiotype antibodies could be causing COVID-19 vaccine induced adverse events and long haul COVID-19
Below in bullet points and pictures, Dr. Niels Jerne’s Network Hypothesis, and mechanism of action will be delineated. Essentially, Network Hypothesis explains what can happen after initial exposure to either vaccinal spike protein, or natural SARS-CoV-2 spike protein. That being, the creation of anti-idiotype antibodies that can then damage the body.
First, 3 prerequisites need to be laid out:
Number one, the antigen causing damage to the body is called spike protein (SP). Someone can be exposed to SP from either the SARS-CoV-2 virus (those spikes coming out of the virus), or vaccination. So, after initial exposure, an individual has antibodies so that the next time they are exposed to the virus, recognition can occur faster resulting in less symptomatic disease.
Number two, it can be said with a degree of certainty that spike protein from both vaccination, and natural infection could be causing 1.) side effects and 2.) long haul COVID-19.
Number three, when SP attaches with ACE2 receptors on human cells, an inflammatory cascade occurs that hastens pathology (disease).
Now that the table has been set and the terms have been laid out, the following literature will explain Network Hypothesis in bullet points and pictures. Keep in mind, bullet points will be broken down into two groups:
🔔 The first group explains how antibodies are normally produced against an antigen-spike protein from vaccine or virus
🔔 The second group explains Network Hypothesis and how anti-idiotype antibodies could be causing damage to the human body
🔬 GROUP 1: HOW ANTIBODIES ARE NORMALLY PRODUCED AFTER EXPOSURE TO VACCINE OR SARS-CoV-2 SPIKE PROTEIN:
SARS-CoV-2 virus with naturally attached spike protein, or spike protein that the body produces after being vaccinated make their way over to a human cell and attempt to attach with an ACE2 receptor (📸FIG. 2)
After getting closer, ACE2 receptor clasps the receptor binding domain (RBD) of SP (📸FIG. 2)
Next, TMPR22S, and FURIN enzymes break the SP head into 2 segments: S1 & S2 (📸FIG. 2)
Moving on, REGARDING SP FROM VIRUS: After the S1 segment is removed by TMPR22S, and FURIN, the remaining S2 segment docks itself on the human cell membrane enabling virus to dump its contents inside the cell which will result in infection. REGARDING SP FROM VACCINE: After the S1 segment is separated from S2 with proline backbone by TMPR22S, and FURIN, an immune cascade begins as T Cell exposure to vaccinal SP stimulates the beginning phases of antibody production(📸FIG. 2)
Finally, the body will begin recognizing SP from either SARS-CoV-2, or vaccine by whats called the innate immune response. This will be explained on the next slide (📸 FIG.3)
Next, a macrophage will be called over to the viral or vaccinal SP unit to consume and digest it. As a result, the macrophage will have an antigen (a part of the SP) so the body can begin making antibodies. That process starts by a macrophage presenting that antigen on its surface (antigen- aka piece of digested spike protein) to a naive T- Cell (📸 FIG.3)
The naive T- Cell in the presence of interleukin 4 (IL4-a cytokine that signals white blood cells/proteins over to either fight the virus or handle the vaccinal SP + also heightens the overall immune response) and in the absence of interleukin 12 (IL12 a similar cytokine), becomes a T helper 2 cell (📸 FIG.3)
The newly born T helper 2 cell releases interleukin 4+5 which activates B cells that are connected to the SP antigen (📸 FIG.3)
Finally, that B cell becomes a plasma cell which in turn produces antibodies against either vaccinal SP, or SARS-CoV-2 SP. The antibodies are those yellow Y looking figures (📸 FIG.3)
At this point it is important to note that antibodies produced by the previously explained process have an identical shape to human ACE2 receptors. As a consequence, instead of the spike proteins from vaccine, or virus fitting into human ACE2 receptors which cause damage, on the contrary, they marry identical looking antibody receptors that neutralize them. Said differently, your body produces antibodies that recognize spike protein and kill the virus during the next encounter. Just so we’re clear, once an antibody is attached to RBD of a SP, a conformational change occurs on the antibody (a physical change) where complement proteins then attach and activate. As a result, said complement activation signals an inflammatory cascade by way of cytokines and other cell mediated signaling methods which alert the immune system of the foreign invader (the viral or vaccinal SP) the antibody is latched onto. Soon after, the alert is reciprocated and the viral unit is destroyed by multiple immune cells. All that would be the normal antibody response.
🚨Another important point as noted in 📸 FIG.4, each antigen specific antibody has an 1.) idiotypic aka variable region which effectively acts as a key possessing a unique shape, that only fits into a specific lock- that lock being SP. In other words, the idiotype or variable region of an antibody is what makes it partial to it’s target🚨
🔬 NETWORK HYPOTHESIS- WHEN ANTIBODY PRODUCTION GOES WRONG AND HARMS THE BODY:
Sometimes the variable region on an antibody can become reversed (NETWORK HYPOTHESIS). To explain, historically, as antibodies variable regions are being constructed during somatic hypermutation and to some degree VDJ recombination which are processes much like a random lottery that decide what an antibodies idiotypic/variable regions will look like and how they will function, an opposite antibody can be produced that damages the body instead of protecting it (📸 FIG.4)
How does that happen? You see, the antibody against the virus, or vaccinal SP RBD can re-enter the previous process explained in 📸 FIG.3. If you remember, the innate immune response against SARS-CoV-2 in 📸 FIG.3 transpired after the macrophage presented an antigen (SP) to a naive T Cell. Well, in 📸 FIG.5, instead of the macrophage presenting a SP antigen to a naive T Cell, it presents an antibody initially produced from the first exposure instead.
Continuing on, that same pathway runs. However, the end result is an antibody which has a lock-like shape of the SP RBD. Said differently, the new antibodies are the reverse of the previously produced antibodies. Importantly, those newly generated antibodies are called anti-idiotype antibodies, or antibodies against antibodies(📸 FIG.5)
As shown in 📸 FIG.6, the anti-idiotypic antibody instead of neutralizing the virus, attaches to a human ACE2 receptor. That attachment unbalances cellular homeostasis and creates systemic inflammation and pathology
🔔 SO WHAT DOES ALL OF THIS MEAN?
It seems there is a chance the body could be producing antibodies against antibodies, which could explain long haul COVID-19 symptoms, vaccine adverse events, and pathology after exposure to both SARS-CoV-2 virus and vaccines. Unfortunately, that is because anti-idiotypic antibodies attach themselves to the ACE2 receptors on human cells. The resulting attachment dysregulates cell functioning which hastens systemic inflammation. Of concern, is the particular type of inflammation. To be specific, ACE2 receptors play a major role in the integrity of blood vessel walls, and in the function of pericytes that help strengthen the vasculature and tissue of the heart, and lungs (to name some)4. So, downregulation of ACE2 by anti-idiotype antibodies can induce vascular damage like micro clots at a capillary level in places like the heart and lungs. That could explain the breathing complication, lung damage, myocarditis, thrombosis, and even thrombocytopenia experienced by people who were exposed to either natural SARS-CoV-2 SP, or vaccine SP. Here’s the biggest problem, those anti-idiotype antibodies, much like normal neutralizing antibodies can remain in the body for months, and even years. That means, damage could be ongoing for quite sometime until the body gets rid of them. Finally, the length of time said antibodies spend in the body (months, years) could explain why long haul COVID-19 is experienced for so long.
📸 FIG.2
📸 FIG.3
📸 FIG.4
📸 FIG.5
📸 FIG.6
🤔 What can be done?
Unfortunately, not much medically can be done at this time. However, some ideas will be listed in bullet points below:
ACE2 blockers (angiotensin converting enzyme) will not work as they don’t directly affect the receptor, only the ACE2 enzymes. Instead, consider the use of xanthenone, and diminazene aceturate (these ACE2 RECEPTOR BLOCKERS not approved for human use yet. Could something be done with them?)
Revisit the idea of getting vaccinated after previous exposure, as anti-idiotypic antibodies could result. Is dose 2 and 3 risky for young healthy individuals because of the previously explained process?
Healthy males under 40, consider passing on boosters, or take Pfizer over Moderna
Consider giving 1 or 0 doses of mRNA, or adenovirus vector vaccines to healthy males under 40, particularly males between 16-30 at highest risk of myocarditis and pericarditis. This seems to result in lesser adverse events and greater immunity
If giving 2 doses to said group, consider spacing doses at least 3 months apart as this also seems to result in lesser adverse events
As spike protein from both vaccination or natural infection seems to be toxic for many people, consider reengineering a vaccine that targets alternative parts of SARS-CoV-2 like N-protein
🔔 SO WHAT DOES ALL OF THIS MEAN?
All and all, it seems we need more treatments for the damage caused by anti-idiotype antibodies brought on by vaccines and natural infection. Possibly, medications that block ACE2 receptors, re-engineered vaccines, and abstention from current vaccine guidance for those at highest risk. Considering all salient facts, a question remains. How was someone you know affected by the vaccine, the virus, or long haul COVID-19?
LETS CONNECT:
https://www.aai.org/About/History/Notable-Members/Nobel-Laureates/NielsKJerne
https://health.ucdavis.edu/newsroom/news/headlines/antibodies-mimicking-the-virus-may-explain-long-haul-covid-19-rare-vaccine-side-effects/2021/11
https://www.nejm.org/doi/full/10.1056/NEJMcibr2113694
https://pubmed.ncbi.nlm.nih.gov/34807265/