On the midwit planet formerly known as Earth, the human immune system is generally believed to suffer a horrific flaw: It refuses to protect itself against SARS viruses. It requires our helping hand, in the form of regular mRNA injections, to encourage it to produce the antibodies against SARS2 that for whatever reason it refuses to produce on its own initiative. And then, by consistently maintaining these antibodies at high levels, we can protect ourselves against this virus.
So the theory goes, the unspoken notion behind all of this insanity is that the immune system requires an alteration, it needs to be provoked into doing something it won’t do on its own initiative.
And in fact, whenever people are found not to produce these marvelous antibodies, all the alarm bells go off. All the midwits freak out upon reading this:
OH NO, THE SNEAKY STEALTH OMICRON VIRUS FOOLS THE POOR RETARDED IMMUNE SYSTEM INTO NOT PRODUCING THE ANTIBODIES THAT IMMUNE SYSTEMS CRAVE!
If only the juvenile immune system were a little smarter, more like that of pensioners, it would realize it needs to constantly make the marvelous antibodies that immune systems crave.
It’s really simple. The innate immune system is the first branch to intervene when a virus shows up. If the innate immune system can’t handle the virus on its own, the adaptive immune system is activated. The reason you see just 18% of children develop antibodies, is because the innate immune system is generally competent enough to deal with the virus on its own. That’s what happens with a relatively mild variant of SARS2, in a relatively healthy child.
In fact everyone commenting on this study seems to skip over the fact that these guys only checked for IgG. The majority of children don’t respond to SARS2 infection with IgG. You can detect an IgM response in them, but not an IgG response.
It’s good not to have antibodies constantly circulating against pathogens like this, because all sorts of risks are associated with that. Those antibodies may for example interfere with the response against pathogens against which they’re not part of an optimal response. And worse, viruses like Dengue evolve serotypes, where one version of Dengue can use the antibodies against another version of Dengue to its own advantage.
Most importantly perhaps, antibodies can interfere with other elements of the immune system doing their work, as documented here for NK cells in influenza. There must be plenty of unvaccinated people now who have IgG antibodies in serum, but that’s a consequence of constant exposure, which is a consequence of a population suffering constant waves of COVID.
And it gets worse. Imagine if you manage to get everyone’s immune systems to produce high levels of antibodies, against a virus that nonetheless manages to keep infecting everyone. You’re going to be selecting for viruses that figure out one way or another, to survive in the presence of those antibodies. And that matters, because the antibody response is basically the last ditch effort we have against pathogens. This whole idea of making the constant circulation of a rapidly mutating virus manageable by giving everyone high levels of antibodies against it is something we don’t do for other pathogens. Only for SARS2 do we pretend this is a way out.
Now have a look at this, a survey in the UK where they look at antibody concentrations in the population:
In contrast, the elderly’s immune systems figured out they need constantly elevated levels of antibodies, because Pfizer’s got what immune systems crave:
So 92% of elderly have antibodies at the 800+ ng level. Well then, surely the elderly must now be safe from SARS2, while the children are dropping dead like flies, right?
You would imagine at some point after enough dead bodies have piled up the midwits start asking themselves whether they bet on the wrong horse, but the thought never seems to occur to them.
But ask yourself: What happens to a coronavirus that continues to circulate in a population despite the high levels of antibodies everyone has against it? It’s going to evolve in a manner to survive despite the presence of those antibodies.
What strategies are available? Pick your favorite:
- Neurovirulence! The brain is protected from IgG antibodies by the blood brain barrier in most people (the blood brain barrier integrity is affected in many mental conditions, which may explain why long COVID is associated with pre-existing mental conditions), so if you focus on infecting the brain, you can continue spreading! BA.5 was the most neurovirulent version of SARS2 seen so far. Pinkeye is a typical XBB.1.16 symptom. Is it now just spreading through the eyes from one human nervous system to another?
- A strong offense, is the best defense. Exhaust the B cells, kill the T cells. This can make future reinfections easier too. India is now seeing a resurgence of measles and chickenpox, so we seem to be going in that direction.
- Molecular mimicry. What happens when those antibodies we’re deploying also bind to our own proteins?
- Glycosylation. Just figure out how to shield the receptor binding domain with sugar molecules, so that the antibodies become useless. Very cool in combination with option 3. And if you can’t figure out how to do it while still infecting through ACE2, pick another receptor. This is one of the ways HIV managed to stop people from developing effective vaccines against it. And it works for Lassavirus too.
- Serotypes: This is getting out of hand, now there are two of them! SARS2 could go for a Dengue strategy: The antibodies induced by version 1 facilitate infection by version 2 and vice versa. As the genetic diversity of spike increases this grows more likely.
- Immune suppression. More than half the genes in SARS2 are linked to interferon suppression. Suppress interferon and you suppress all sorts of downstream molecules that eventually alert the T cells, which alert the B cells. This is the Ebola strategy: Before the immune system figured out anything is wrong you’re already everywhere, because you were suppressing all the warning signals.
- Immune suppression through molecular mimicry! The lovechild of option 3 and 6. SARS2 is capable of inducing antibodies against interferon and other cytokines. So through the magic of evolution, SARS2 can induce an antibody response against itself, that also binds to the proteins that are supposed to stop SARS2 from replicating, or are supposed to warn your immune system of the infection.
- Super receptor affinity! If your Spike protein’s affinity to a receptor is strong enough, you can bind to your receptor before antibodies can bind to your Spike. And again, if you can’t pull this off for ACE2, try it for another receptor. I think the main problem prohibiting this route is that it would start binding to red blood cells, but I could be wrong.
- Cell to cell transmission! If you simply move directly between cells, neutralizing antibodies can’t reach you. SARS-COV-2 is already quite capable of this and it can learn to get better at it.
As Homo Sapiens Sapiens decided the way forward would be through a sustained wall of antibodies, at levels unlikely anything provoked by natural immunity, you’re forcing this virus to embark on exotic journeys to survive. And although I like to think of myself as smart, I’ll be honest: I don’t know which of these exotic journeys works best. I just know there are plenty plausible routes and they all lead to SARS2 surviving by making the disease course worse.
Previous generations of public health officials did not say “well everyone now has antibodies against smallpox, so smallpox should be mild from now on”. The vaccine stopped you from getting smallpox. Same for measles, polio and just about all the other vaccines. You don’t want a virus to continue evolving in the presence of antibodies against it. That’s how you make the virus more dangerous.
NK cells preferentially deal with virulent varieties of influenza. Imagine for a moment how great it would be, if you had allowed your tissue-resident NK cells to do the job they’re supposed to do: Check how cytopathic the virus is before they decide whether to kill the infected cell.
I can show you a route that facilitates evolution of reduced virulence: NK cell immunity.
But the route that humanity chose, survival through population-wide constantly elevated levels of antibodies in serum, your body’s last option when innate immunity and the T cells can’t do the job on their own, what path does that send a sarbecovirus down?
Antibodies are an emergency measure of last resort. When you constantly force a virus to evolve in the presence of your emergency measure of last resort, whose fault is it when these viruses evolve to become more virulent, by overcoming your emergency measure of last resort? I’m really sorry, but it’s not me who decided to violate basic principles of immunology and evolution.
I can show you how the route you chose encourages increased virulence, I just did. Who can show me how constantly elevated levels of antibodies in serum facilitates the evolution of reduced virulence?
And I know what some of you will ask: Well what about all the other viruses that infect us? Why doesn’t Adenovirus #421 suddenly pull a scary trick out of nowhere?
Well friends tell me, how many of those viruses continue to circulate in the presence of a constant wall of antibodies? If everyone was constantly getting infected by measles twice a year, despite a big wall of antibodies, I’d be worried too.
Vaccination against respiratory viruses is a trial and error process. They tried it against Respiratory Syncytial Virus in children, they killed and hospitalized a bunch of kids with it, so they stopped. They tried it against influenza, it kind of seems to work in old people when you vaxx them a few weeks before the wave (until it stops working once OAS kicks in after a few years of annual flu shots), so they keep doing it.
A lot of people do have antibodies against seasonal influenza, but seasonal influenza doesn’t have the genes for potent interferon suppression. Sarbecoviruses are very good at interferon suppression, more than half of the SARS2 genes are involved in interferon suppression, so the capacity for improvement is there.
And in addition to this, you can just check viral biomass in sewage. The only thing that seems to come close to SARS2 in our poop, is a plant virus from our food. Other viruses don’t circulate at these levels. And without persistent infections and a high viral biomass, you don’t get to mutate very rapidly.
And the other human respiratory viruses that regularly infect us don’t have the wide tissue tropism SARS2 has either, they tend to stick around in the epithelial tissues in our upper respiratory tract. That’s part of the reason they’re good at reinfecting us: They almost never anger the immune system enough to provoke an antibody response that prohibits reinfection for any sustained amount of time.
Rather, what prohibits reinfection for them tends to be our innate immunity and their competition with other respiratory viruses for the same tissues, not the whole population suddenly having high levels of antibodies against an obscure rhinovirus. That’s not how this is supposed to work.
There are different ways this could end, but what I don’t see happening is what all the midwits who peddled these vaccines now promise, a situation of endemic SARS2 circulating at low levels. India just very clearly illustrated we’re nowhere near an endemic SARS2 situation. We’re now entering a period of increased virulence due to improved interferon suppression. This will mainly affect people whose NK cells have not received training, as the NK cells don’t require interferon to figure out a cell is infected.
This could lead to a situation where constant reinfection just reduces immune pressure by constantly killing off and exhausting their lymphocytes. You could also start to see antibody levels so high that people start suffering autoimmune problems, amyloidosis and other conditions as a result. We’ve never seen what’s happening now before, it could cause unprecedented problems.
But what seems most likely to happen if you want to go with van den Bossche’s prediction, is that eventually, after we have these novel variants with improved interferon suppression circulating through the population, the wall of antibodies surges higher until it limits transmission again. And then after a moment where the virus seems to vanish, we start to see heavily glycosylated versions of SARS2 emerge from persistently infected people, that cause the antibodies to become altogether useless.
At the time of Omicron, antibody evasion would have been a useful strategy. But the reality we now live in is a population that has very high antibody levels, as well as an increasingly heterogeneous response due to different people getting infected by different strains. Under those circumstances there is no strong growth advantage to be had anymore by subtly mutating the receptor binding domain. In the past, variants that developed a growth advantage by mutating the interferon suppressing genes were generally defeated in the quest for global dominance by variants that changed spike, so until now, this was a dead end strategy.
Similarly, we still live in an era in which heavy glycosylation of spike is a dead end strategy. Variants sometimes emerge that show changes seemingly leading to increased glycosylation, but their growth advantage is not big enough compared to variants that deploy other strategies, so they go extinct again. Interferon suppression right now seems to be the lowest hanging fruit that’s getting harvested.
But how long does that last? It would be expected to last until we reach the next stage, when improving interferon suppression runs into the territory of diminishing returns, like spike mutation is running into now. Antibody evasion through increased glycosylation probably comes at the cost of reducing ACE2 binding affinity, so you’d need variants with strong ACE2 affinity, that are placed under extreme pressure by a heterogeneous range of antibodies and can no longer sufficiently evade those antibodies by improving interferon suppression.
What happens once the Spike protein becomes heavily glycosylated? To deal with glycosylated antigens, the body tends to rely on IgM, our largest antibody, rather than the IgG induced by vaccination. It’s hard to bind strongly to these antigens covered by sugar, but by having many places at which it binds simultaneously, IgM can still bind and provide some interference.
IgG on the other hand is specialized in binding to proteins, which is exactly why viruses tend to have their outside proteins covered in sugars. The other coronaviruses are covered in sugar molecules too. If IgG always beat IgM to the race in binding to proteins, then IgM never underwent affinity maturation, that is, the body never figured out how to develop an IgM that binds really well to SARS2 Spike proteins.
And worse, if the IgGs keep binding strongly, they can stop IgM from binding. So what you would expect is that over time SARS2 starts rearranging its sugar molecules, in a manner that prohibits the IgGs from binding where they interfere with binding to the receptors, while allowing them to bind in places where they would interfere with IgM and (perhaps) IgA binding.
And I will illustrate this again, the vaccine screws up the antibody response, by not stimulating IgM, while readily stimulating IgG:
The binding intensity of serum IgA and IgM 30 days after the second mRNA vaccine dose remained low to negligible for both vaccinated healthy donors, with binding to S proteins at similar intensity levels as previous exposures to endemic coronavirus NP for IgA (Fig 9B). On the other hand, IgM binding to S antigens was lower than to endemic coronavirus NP (Fig 9C), indicating essentially no IgM response to the mRNA vaccine. These data suggest that vaccination with mRNA for S protein or protein fragment did not elicit the same substantial IgA and IgM response as SARS-CoV-2 infection.
As far as I can tell, IgM really just needs to see viral particles in your respiratory tract to learn to fight. It’s found in blood and in mucus, but if the first exposure is to spike on proteins expressed in a deformed shape, with abnormal glycosylation (because the other viral proteins are lacking), on the surface of a cell somewhere in your arm muscle, then IgM is at a big disadvantage compared to IgG. And so that would mean regardless of whether you go for peptide vaccines (Novavax) whole inactivated (Chinese), Adenovirus junk or mRNA junk, IgM is prohibited from joining the fight.
The above study also found no decay of IgM and IgA relative to IgG over time after infection. We also know the antibodies in breast milk are IgA in the naturally immune, but IgG in the vaccinated. And it’s not just a matter of multiple exposures naturally shifting the response from IgM and IgA to IgG. The body still responds with a surge of IgM during SARS2 reinfections. This also fits what they see for influenza in mice, where it’s IgM that remains responsible for protection. But the midwits seem to think IgM is some sort of “learning antibody” on the way towards the holy grail of IgG. It’s not.
It’s IgM that would normally kick in first and reduce the viral load by multiple orders of magnitude. You want this for multiple reasons: It’s not going to provoke autoimmune problems, it’s not going to generate mutants, it’s not going to pass through the placenta and screw up a developing fetus, it’s too big to be abused for antibody dependent enhancement mechanisms and most importantly, it’s a very potent neutralizer, because it happens to be so big. By pulling on different places at once, it deforms the shape of the protein it’s binding to.
Then after that has happened, IgG begins to climb, generally due to IgM producing B cells that did a good job at controlling the virus switching to IgG. Its main role is not to neutralize the viral particles, but to point out the infected cells that were producing the virus, so that those cells can be destroyed. This role of course is what you screw up dramatically, when you provoke a tolerogenic immune response that leads to IgG4 antibodies. When those antibodies bind to viral peptides found on the surface of infected cells, your NK cells and CD8+ cells don’t interpret them as a signal to kill those infected cells.
That’s how this thing is supposed to work. That’s how nature managed to give rise to vertebrates like us, that can live in high densities and cope with regular infections by rapidly mutating respiratory viruses. The human body produces the antibodies it needs, when it needs them. The absurd situation of a whole population having a sustained wall of antibodies in an effort to make a virus mild as it continues infecting them twice a year is something you don’t see in nature.
In vaccinating everyone, the midwits violated every rule in the playbook. That’s going to backfire, dramatically. I warned about this, not because I’m so eager for a doomsday scenario (read back march 2020 if you think so), but because what they’re doing didn’t make sense. It already has backfired. It’s not normal for everyone to get infected twice a year by a sarbecovirus. It took less than a year for a variant to emerge that got around the artificial homogeneous antibody response, guaranteeing we’d be stuck with constant high waves of infection.
If we have plunging life expectancy, persistent excess mortality concentrated in the most vaccinated nations and increasingly showing up in younger age categories, a labor force with record sick leave, a rising disability rate and plunging labor productivity, all together resulting in persistent high inflation, why does everyone insisting on pretending they solved the problem? Only idiots would pretend this is success. But they’ll have to stop pretending soon.