I’ve explained through a few posts now, how SARS-COV-2 responds to the population’s antibodies, by adding sugar molecules (glycans) to regions targeted by the antibodies. This is how viruses tend to evolve to resist antibodies over time, regular influenza (H3N2) has been slowly doing this in response to mass vaccination of elderly and HIV gradually does it within a person over a period of years.
There are studies that look at what happens when you add glycans to a virus. Generally the innate immune system gets a bit better at handling the virus, whereas the antibodies become useless. But it’s hard to completely simulate what happens in the lab, not in the least of reasons that in the wild, you’re dealing with a quasispecies swarm. This is what we call it, when many different mutants, each with slightly different traits, circulate together and jump from one person to another together.
This has the effect of increasing its ability to sicken people, through various methods. One version may be better at infecting certain tissues and organs than the other. One version may optimally replicate at 38 degrees, another may optimally replicate at 39 degrees. The fever induced by the prior then aids the latter in replicating.
That’s what goes on with SARS2. About half the detected samples evade antibodies on the N1 loop by putting a glycan at position 22, the other half evade antibodies by putting a glycan at position 30, by deleting S:31. They both replicate optimally at slightly different temperatures, so having them circulate together probably increases virulence.
The SARS2 swarm of different variants grows increasingly virulent over time as it diversifies, but sometimes it has to start from scratch again. When Omicron emerged, it started from scratch again, losing its genetic diversity. This played a role in causing the virulence to suddenly drop. About a year ago, antibodies emerged against the N1 loop in the NTD, that were very difficult to overcome. This again forced the swarm to start from scratch, with BA.2.86, which spread across the globe once it added two further mutations to turn into JN.1.
As time goes on, it becomes harder for the immune system to find some region to target with antibodies that will work on the entire swarm. It happened twice so far, but there’s no guarantee the whole swarm will have to start from scratch again at some point in the future. The first time such a global reset happened, it also proceeded much more rapidly than the second time.
So when it comes to understanding how vaccination will impact what’s going to happen, I think it’s useful to look at the experiment of vaccinating chickens against H5N1 again. We know what the virologists fear, by what they decide to experiment with. Whether it is wise for them to engage in their experiments, is a different question.
As an example, have a look at this experiment, where they decided to apply what we may now refer to as the van den Bosschean horror scenario to H5N1: They edited the virus, to put glycans on every position where you can expect antibodies to bind. You can ask yourself, if it’s wise to experiment with creating such a virus. I think it’s not, but linking to the experiment won’t undo the experiment.
What you see is that yes, when you fully cover H5N1 in glycans, you end up with a virus that escapes the vaccine induced antibody response against it, both in vitro and in vivo. It is however, not an inherently very virulent virus when you cover it in these glycans, because the innate immune system evolved to recognize viruses pulling this trick. To make the virus actually scary under these conditions, you have to get rid of the cellular immune response.
You have to remember, that the experiment of putting glycans everywhere, is not identical to what happens in nature. Yes, viruses respond to antibodies by adding glycans. But they also add other mutations, that compensate for the structural changes induced by the glycans. And of course, they evolve different variants of their proteins, that add the glycans on different positions (the quasispecies model).
But what I find far more interesting myself, is what happened in Egypt, where they’re dumb enough to vaccinate their chickens against H5N1:
Studying the progressive genetic changes in A/H5N1 after long-term circulation in poultry may help us to better understand A/H5N1 biology in birds. A/H5N1 clade 2.2.1.1 antigenic drift viruses have been isolated from vaccinated commercial poultry in Egypt. They exhibit a peculiar stepwise accumulation of glycosylation sites (GS) in the haemagglutinin (HA) with viruses carrying, beyond the conserved 5 GS, additional GS at amino acid residues 72, 154, 236 and 273 resulting in 6, 7, 8 or 9 GS in the HA.
So yes, in the vaccinated Egyptian chickens, we see the van den Bosschean doomsday scenario. There is a “peculiar stepwise accumulation of glycosylation sites” observed, in the main protein targeted for neutralization. There’s no clear evidence of decreased or increased virulence of these viruses: They generally just keep killing every single chicken they infect. There’s also no apparent detrimental impact on the transmission of these viruses, except for the very last glycan added.
The purpose of these glycans, appears to be to allow the virus to persist in its host. In mice we also see that the new glycans that started emerging in human influenza a few years ago, have the effect of increasing replication of the virus, virulence and antibody evasion.
It’s worth noting, that despite an increase in vaccination of elderly against influenza, we’re not seeing a decline in influenza deaths. In 2018, before the SARS2 pandemic starts distorting everything, the United States had the most influenza deaths since the 1967-77 season. This despite about half of elderly being vaccinated. It seems influenza evolves in response to vaccination, to become deadlier.
Of course, with far less of the population being vaccinated against influenza and with most of the people who are vaccinated having been infected by influenza many times before they received a vaccine against it, the selective pressure on influenza is less intense than it is for SARS-COV-2. In addition, SARS-COV-2 is inherently just a nastier virus than influenza: SARS2 can infect endothelial cells, it can kill T cells and it can draw T cells into the brain. Normal season influenza can’t do any of this.
SARS-COV-2 is evolving very rapidly for a corona virus and as I’ve mentioned before, we notice that it’s rapidly adding these glycans. JN.1 mutated to add a glycan at either S:30 by deleting S:31, or by adding it on S:22. That puts the glycan on the N1 loop.
But now we see the next glycan emerge, on 188, by changing 190 to Serine or Threonine. The version that’s now conquering the world is called LP.8.1. It adds the glycan on 188 and changes some amino acids next to it to adjust to the new glycan. But then it takes a next step. It changes S:679 to Arginine, which further improves the polybasic Furin cleavage site, by adding another basic amino acid. That’s now the most rapidly spreading version.
I first pointed this out a year ago that it was improving the furin cleavage site, but those lineages were unable to compete against lineages that added new glycans. But now we see a lineage that added the glycans and on top of that, now improves the furin cleavage site.
And some of you may wonder: Why keep track of every little detail? Who cares about any of this? Well, this virus is out there, damaging brains and immune systems of everyone. There’s an entire generation of children constantly getting reinfected by it.
We know what we see in chickens, with influenza: When you vaccinate them against it and they keep getting infected with it, the virus gradually evolves to evade the antibodies and merely grows more virulent. H5N1 now kills 90% of chickens within 48 hours.
And quite frankly, I don’t like what we’re seeing. This is how many people in Denmark catch mycoplasma pneumonia now:
If this is immunity debt, it comes with one hell of an interest rate. In Japan they’re seeing record breaking numbers of cases too, unseen since they began tracking numbers in 1999. Mycoplasma pneumoniae is the second most common cause of pneumonia.
So what’s the perpetrator? The lockdowns are being thrown under the bus right now. But as I warned about long ago, nobody really knows what happens when you have an IgG4 response in the lungs to a common respiratory virus. And then there is the fact that the immune system has to devote its limited T cell capacity to one single new virus. And then on top of that, you’re dealing with a virus that kills T cells and of course irritates the lungs.
But I want to point out again, that a natural infection by a new virus, will lead to a balanced immune response: The innate immune response is strengthened through exposure to such a virus. This innate immune response can handle very different viruses roughly equally well. As an example, you see that an infection by SARS-COV-2, improves the ability of the alveolar macrophages in the lungs to subsequently protect the body against Influenza.
Only when the innate immune response can’t handle it on its own, is an antibody response produced to a novel agent. But after vaccination against SARS2, antibody concentrations are about 50 times higher than after natural infection. So we shifted the balance in the lungs of most of the population, towards a highly specific adaptive immune response, targeted at SARS2.
You can go back and read my posts about all of this, back in 2021 and 2022. I warned you that we were at risk of seeing all sorts of other respiratory pathogens start to take over in the lungs, because the immune system was stuck with this abnormal adaptive response targeted at SARS2 and the innate immune response was suppressed.
Now we’re stuck with a world where everyone is just coughing all the time. Queen Camilla, King Charles wife, can’t show up in public because she has a cough that just doesn’t go away and feels tired all the time.
I warned you about all of this. You can’t expect the adaptive immune response to keep this virus under control for us. The innate immune system has to deal with rapidly mutating respiratory viruses of this nature. The adaptive immune response, has the job of discriminating against virulence associated epitopes.
That’s what the antibodies are supposed to do: Imagine your neighbor catches a mild virus of SARS2 and you catch a nastier version. You’re both of similar age and overall health. You will have higher antibody concentrations as a result and they will react more strongly with your version of SARS2, than with the version your neighbor caught.
This then gives a selective advantage to the milder version your neighbor caught, because it stands a better chance of reinfecting you, than the nastier version you caught. You see this in survivors of the 1918 pandemic influenza: They have highly evolved antibodies against it (affinity maturation), that only react with the 1918 virus, but not other influenza variants. That’s why we did not end up stuck with endless waves of very nasty influenza: The survivors gave the nasty influenza a survival disadvantage, through their adaptive immune response.
All of this could have been avoided.
Very interesting and informative post, thank you.
> The purpose of these glycans, appears to be to allow the virus to persist in its host.
Vanden Bossche posted a recent article (29th November) on his (now pay-walled) Substack in which he talks about the glycosylation of the N-Terminal Domain. Honestly, the article was very difficult for me to understand but there was one part that really took me by surprise. I quote:
“I do not concur with the notion that SC-2 causes chronic infection. I believe instead that the repeated detection of the virus is due to prolonged adsorption of SC-2 to patrolling DCs in the URT.”
Dr. GVB is obviously aware of the class switch from IgG3 to IgG4 induced by the mRNA vaccines. You’ve described many times how these tolerogenic antibodies prevent various branches of the immune system from killing infected cells. Yet GVB doesn’t believe that this would be causing widespread chronic COVID infections? That’s a little strange.
And you also have to consider the wastewater data. You’ve shared this graph before, showing SARS-CoV-2 concentrations in San Francisco sewage:
https://www.rintrah.nl/wp-content/uploads/2024/08/1areaundercurve.jpg
You can clearly see that many of the viral “lows” in wastewater from 2022 onwards are even HIGHER than the viral “peaks” during 2020 and 2021, which seems to suggest a significant percentage of the population suffering from persistent infections. I recall the “variant trackers” on Twitter recently discussing case reports of people with THREE YEAR persistent Delta infections.
So, if GVB was correct about the virus being confined to the upper respiratory tract and not persisting elsewhere in the body, then we wouldn’t be seeing massive amounts of virus in the sewage. Don’t get me wrong, I really like Geert, he is a hero for sounding the alarm, but he does seem to examine things in a very “black or white” way if you know what I mean.
So I am starting to lean more towards your predictions, that these future variants with glycan shields will resemble something more like latent TB or HIV rather than a highly virulent virus that people will succumb to very quickly (as Geert is predicting). But obviously it’s impossible to predict with 100% certainty what’s going to happen. Only time will tell.
Yeah GvdB diverges from consensus in a lot of peculiar ways:
-Doesn’t think CD8 t cells kill infected cells.
-Doesn’t think persistent infections in immunocompromised people lead to new variants evolving.
-Thinks immunity in the vaccinated now depends on polyreactive non-neutralizing IgM antibodies.
-Doesn’t seem to want to acknowledge long COVID is a serious problem in vaccinated and unvaccinated people.
-And now apparently doesn’t think this virus causes persistent infections.
As much as I appreciate his willingness to warn about the risks of mass vaccination against this virus, I’m not convinced of all these esoteric hypotheses.
Nobody is right all the time. Keep in mind, GvdB also didn’t anticipate the IgG4 problem.
Vaccination has been a mistake, but what the exact consequences will be remains to be determined.
My expectation is it will look like what we’ve seen with H5N1 in chickens: Steadily rising virulence and increased glycosylation, as the population gradually suffers an increase in all sorts of respiratory infections and infections by SARS2 become increasingly persistent.
Hopefully younger and unvaccinated people will benefit from the apparent increased vulnerability of highly glycosylated variants to the various mechanisms of the innate immune response.
I’m not a specialist in biology… but I have a good experience with predictions for various markets and social phenomena.
The typical correct prediction, in most cases, starts its lifecycle with an astute observer noticing an profound imbalance / structural problem. The respective observer is so enthralled by this correct insight, that they expect the spectacular unwinding of the imbalance to occur very soon!
However, there is no guarantee about how many grains of sand one can pour on top of the pile before an avalanche starts. Sometimes, it can take quite a long time. If this is the observer’s first rodeo with a spectacular real-world prediction, they will usually err on the side of “soon” and “spectacular”. Hence GVB’s wishful thinking for a fast, acute course of the process.
In reality things seem to draw out forever. The 2008 market crash was such a phenomenon. There were crowds of observers endlessly waiting for it since June 2005. It was a textbook real estate crash, causing loan defaults and bear market in stocks. Observers were proven correct, but boy, did they have to wait…
Smart people use this bonus time to prepare.
>The 2008 market crash was such a phenomenon. There were crowds of observers endlessly waiting for it since June 2005. It was a textbook real estate crash, causing loan defaults and bear market in stocks. Observers were proven correct, but boy, did they have to wait…
Yep. And shorting it almost went wrong for Michael Burry.
These evolutionary developments are very concerning and scary.
If only the mad “health” scientists would stop playing devil!
I live in Hawai’i and many of the people I know are coming down with a bad and prolonged cough that takes a month or more to go away or that lingers even longer. There are kids who normally don’t get sick at all missing weeks of school with pneumonia this autumn. I have also seen evidence of a drop in the ability to understand basic concepts and an unmistakably massive decline in motivation among the students in last few years.
When they ask me for health advice, I tell them to eat lots of organic raw garlic.
I use the Sperti Vitamin D Sunlamp. It’s the only FDA-approved lamp that produces the right wavelengths for Vitamin D. Sperti has several products, only one of them is the Vitamin D one. Confirmed by clinical study and by my own bloodwork before and after, during winter. Nobody cared about it back in 2021 when I ordered it, but now it’s on backorder for some reason.
Non-biologist here, trying to understand the quasispecies swarm concept… Am I correct to understand that any of the variants under discussion (LP.8.1 for example) are actually a quasispecies swarm? And when the pathology of a variant is being discussed, the effects on the lungs are coming from one member of a family, but the effects on the digestive tract may be coming from another member of the family? And when the physical/chemical structure of a variant is being discussed (i.e. what glycans go where, etc), it is the shared characteristics that are actually being discussed, captured with statistical methods? Or whatever member of the subspecies the researcher happened to capture in their analytical apparatus)?
Or does the quasispecies swarm mean that LP.8.1 is circulating together with other named variants, and when someone “catches” LP.8.1. they are also infected with other named variants too?
In any case, I remember Sirotkin noting back in 2021 or 2022 that the Chinese were running anal swabs on visitors entering the country, because that’s where evidence of all members of the quasispecies swarm is being collected. Unlike throat swabs, that would not catch variants hiding in the digestive tract.
>Or does the quasispecies swarm mean that LP.8.1 is circulating together with other named variants, and when someone “catches” LP.8.1. they are also infected with other named variants too?
Yes, this is correct. People will tend to be infected by multiple variants, but depending on how you test, you will just find a small subset of those variants.
I think they will look like FIP.
Hi Rintrah,
I know this is an old post but it’s your newest regards covid and Sars-CoV-2.
Have you seen this tweet from yesterday (15th December) re: fast rising US covid levels:
https://x.com/michael_hoerger/status/1868550160105841149
Particularly pertinent from it:
“* Highest % increase in transmission in nearly 3 years
* 10th wave is the “silent surge,” coming on late out of nowhere
Out of nowhere and transmission increase in one week is highest since Omicron stormed on the scene. That’s got to be a concern – do you agree?
And this from Finland (where they vaccinated kids from the age of 5) – yowsers 🙁 :
https://x.com/jukka235/status/1867853170430603746
“Finland’s epidemic 14 Dec 2024: infectious diseases are showing very strong growth. Among 5-24 year olds, infectious disease incidence (ytd) is up to 4-5 times higher than in 2023, and the year isn’t over yet.”
This is looking at Whooping Cough, Mycoplasma and Adenovirus. Not even flu or covid.
What d’ya think?
>Out of nowhere and transmission increase in one week is highest since Omicron stormed on the scene. That’s got to be a concern – do you agree?
Yeah, not sure what to make of it. It’s a very sudden and rapid increase, but from a low baseline.
>And this from Finland (where they vaccinated kids from the age of 5) – yowsers ???? :
Yeah this is basically what I’ve been reporting on for a while now: Basically the whole population has a mild degree of immunodeficiency now.
The governments mostly manage to mask the problem in the statistics, through a number of methods:
-Paxlovid and monoclonal antibodies for the elderly. The price we will pay for that is further genetic diversity of the swarm, but for now it helps them keep elderly out of the hospital.
-Record levels of mass immigration of healthy young people into Western countries has the effect of reducing excess mortality numbers, as an immigrant has a mortality risk of about 50% below that of a native citizen of the same age.
Anytime you target a single protein of this virus, you’re setting yourself up for failure, followed by an increase in genetic diversity of the swarm.
They keep making the problem worse, but they don’t really care, because the system is run by old people like Fauci who just want to kick the can down the hall by a few years.
But when they’re dead, they’re leaving today’s children behind with damaged brains and immune system.
The purpose of the antibodies is to select against virulence associated epitopes. When you abuse the antibody system to keep the elderly alive, you’re just encouraging the selection of highly infectious variants that are able to infect the children. Note how the first Wuhan variant was unable to infect children. It’s a consequence of continually vaccinating all the elderly that these highly infectious variants now have such a massive fitness advantage.
Comprehensive reply – thanks.
Couple of thoughts/questions…
Do youngsters have more of an issue than unvaccinated adults with these illnesses (even if the youngsters are unvaccinated)? I’m not clear on this aspect though guess it’s all to do with innate immunity. I’m sure being elderly is probably not great in all of this.
As regards the U.S. rise, I am a little concerned that the next stage in the evolution of ‘chronic’ infection capable sars-cov-2 is just making itself known. It’s possibly unsurprisingly that Canada and the U.S. would be the hotbeds for this stage. GvB has linked to an interesting paper that supports the idea of the development of the virus within heavily vaccinated, probably elderly, individuals:
https://onlinelibrary.wiley.com/doi/10.1002/jmv.70107
“Multi-Organ Spread and Intra-Host Diversity of SARS-CoV-2 Support Viral Persistence, Adaptation, and a Mechanism That Increases Evolvability”
Can only see the abstract but that’s quite informative. What d’ya think?