I’ve made a number of posts by now, where I outlined what I consider to be the main problems that led to the vaccines exacerbating the SARS-COV-2 pandemic. What I consider my best post on this subject so far, can be found here. As far as I am concerned, the biggest problem with the vaccines we deployed is that they trigger mainly an IgG antibody response, whereas the natural pattern for our body is to deploy an IgM antibody response against rapidly mutating respiratory viruses.
The higher affinity of the IgG antibodies deployed against this virus then prohibit affinity maturation of our IgM antibodies. To put it in simpler terms: You have big antibodies (IgM pentamer/hexamer) and you have small antibodies (IgG monomer). The big antibodies have a bunch of parts that bind to a virus particle, but to improve the binding quality, these antibodies first need to get to do their actual job. You start causing problems, when you induce an antibody response with the small antibodies, that lead to many of these small antibodies tightly binding all over the virus and prohibiting the big antibodies from binding there, to gradually improve their own binding quality. If the big guys lose the race to bind at the start, they miss out on the opportunity to get better as time goes on.
This particular problem, is a problem I would mainly expect to see among those people who had never really been exposed to this virus before they were vaccinated. There are other problems with this vaccine, that seem more independent from moment of exposure. As an example, the antibody dependent enhancement of infection problem seems more independent of previous exposure: We know the antibody repertoire looks similar regardless of preceding infection history, with binding on locations like the N-Terminal Domain, where a conformational change is induced that serves to enhance infection.
What I wish to explain today however, is how the population got stuck with this IgG dominated antibody response. The reason for that is relatively simple. There is a difference between the big IgM antibodies and the small IgG antibodies. The IgM antibodies generally can’t enter into your tissues. These antibodies exist in your blood and they show up in your lungs and other mucous membranes, but they’re not supposed to show up in the rest of your organs.
This is useful for a number of reasons. As an example, their inability to pass the placental barrier ensures that when a pregnant women gets infected by a respiratory virus, the baby doesn’t have to end up exposed to a bunch of antibodies that can bind to its tissues and cause harm: The IgM antibodies get rid of any viral particles showing up in blood, so the woman and the baby are protected. If you were to have an IgG dominated antibody response against such a virus, these antibodies would pass the placental barrier and show up in the baby, who may very well suffer a degree of harm from these antibodies.
With these vaccines, we expose your immune system to the Spike protein in a position where you would normally not expect the Spike protein to show up: In the Deltoid muscle. To get rid of this alien protein there requires penetrating deep into the muscle, where the IgM antibodies normally don’t reach. And so in the race to bind to this Spike protein, the IgG antibodies have a strong advantage.
This is especially true for the Adenovirus vaccines, which are good at infecting the muscle cells. The mRNA vaccine lipid particles seem to go more for endothelial cells than the Adenovirus vaccines. What we see as a result is that the Adenovirus vaccines are even worse at inducing an IgM response than the mRNA vaccines.
A natural mild infection tends to focus on antibodies against the Fusion peptide, which is a great strategy. The vaccines on the other hand have a broader response, against the NT domain and the CT domain, but with a uniform escape pattern (meaning it’s very easy and useful for the virus to evolve around this response by changing these regions). With sufficient shots, you also start to see a response all over the receptor-binding domain.
That’s great right, those antibodies will stop binding to the ACE2 receptor? Well there’s the thing: Of course that would stop binding to the ACE2 receptor, so the original variant of the virus that spread everywhere and the vaccines are based on evolved in a way that makes it costly for your body to deploy antibodies against the Receptor Binding domain: That whole region is full of sequences found in your own human body, so a broad and strong antibody response against that region would risk all sorts of autoimmunity problems.
Why do these vaccines have such high rates of adverse effects, which get worse with further shots? One reason is because we’re trying to induce an immune response against a version of the virus that was somehow very good at resembling our own protein structures. Natural immunity, when it bothers to target the Receptor Binding Domain, focuses on those parts of it that for whatever reason happen not to look like endogenous proteins in the particular person who is developing this natural immune response. This differs from person to person and so it’s much harder for the virus to escape those responses.
As time went on, the changing antibody repertoire of the human population encouraged SARS-COV-2 to evolve in a way that increased ACE2 affinity, while reducing its resemblance to our own proteins. This is good for us, it means our IgM antibodies can pick out more parts of the RBD to develop immunity against, but this of course only happens if you’re not stuck with a high affinity IgG dominated antibody response that binds to places where IgM would like to bind.
We’re now stuck with the tragic situation, where entire populations are stuck with IgG dominated antibody responses, that are often autoreactive (everyone shows signs of cardiac damage upon vaccination) and most importantly: ARE RECALLED EVERYTIME YOU’RE EXPOSED TO THIS VIRUS AGAIN!
Have a look at an example of the problem we’re dealing with: People who get infected by this virus, develop antibodies that are cross-reactive with brainstem antigens. However, because you have a blood-brain barrier, the IgM antibodies never reach those brainstem antigens, whereas the IgG antibodies against those regions do reach the brain stem. As a result, we see that the IgG antibodies are associated with damage to the brain stem resulting in breathing problems, whereas the IgM antibodies are not.
It’s worth asking yourself this: We have a bunch of young women now who have been exposed to three shots of these vaccines, stuck with an IgG dominated antibody response that is cross-reactive with a bunch of human antigens. These antibodies can pass through the placenta, which the IgM antibodies your body would normally deploy can’t do. What will happen to their children? My expectation is that these women will give birth to children with autism and other disorders associated with brain inflammation at a higher rate than before, among other problems.
The strangest thing is that with constant repeat vaccination, we’re now reaching the point where the IgG antibodies in the vaccinated are switching from IgG3 to IgG4, which is normally the least common IgG antibody in human serum. These are anti-inflammatory antibodies that don’t activate complement and are generally associated with immune tolerance.
In other words, the IgG dominated immune response of highly vaccinated people is starting to show signs of simply tolerating the virus, instead of performing the important role that IgG antibodies normally do of ringing the alarm bells for the rest of the immune system.
I have to ask: What do people think is going to happen, when we have a bunch of people whose immune systems learned to tolerate the Spike protein? I expect it would go a long way towards explaining this:
Along with the mysterious pattern of Paxlovid rebounds in the constantly boosted.
I just can’t emphasize this enough: These midwits fooled the human immune system into deploying the wrong tool for the job, by inducing a first exposure to the Spike protein in a place where the IgM antibodies can’t reach. When you study nature very closely, you’re supposed to develop great respect for its minute details. When you fail to have such respect, then you start causing trouble.