As I’ve said before, the biggest risk in the folly of vaccinating people against SARS2 is the serotype scenario: A situation where two or more versions of the virus circulate simultaneously and immunity you developed against one version merely helps another version make you more ill. The risk of serotype formation increases with time. To prevent this you want to see variant independent immunity, which no currently available vaccines deliver.
We can see the serotype scenario at work for Dengue. Dengue has been around for centuries, but it’s only really after the second world war, when global deaths and severe disease from Dengue begin to climb. The main reason this happened is because air travel now allows the different Dengue versions that evolved to spread around the world. This means that the number of people getting reinfected by a different version at some point in their lives has massively increased.
A second Dengue infection is 9 times more likely to cause symptoms and 24 times more likely to result in life-threatening conditions. The result can be seen in Brazil, where deaths from Dengue went up a hundred-fold over thirty years, as different versions began to circulate in the country together.
Now the question you may have is: If this serotype scenario is such a big problem, why don’t we see it with influenza? Why hasn’t influenza evolved into four different versions that use our antibody response to wreak havoc? Well, that brings us to our good friends we have discussed before, the Natural Killer cells. These cells prevent the immune response from being overly damaging against influenza. They have also been found to dampen the adaptive immune response developed against mycoplasma respiratory disease.
There is also the important difference in variant-independent IgM antibodies mentioned before. These antibodies normally perform most neutralization against influenza and SARS2. But perhaps most important is the simple fact that it just takes a very long time before you catch influenza again: Only about 10% of people catch it and develop a symptomatic infection in a given year.
With far more time between infections, there’s far less incentive to evolve such serotypes. After all, once influenza shows up in your lungs, the immune landscape it encounters won’t be imprinted by the most recent influenza infection you had, but by a hCov or some other pathogen.
In this sense, serotype formation is also encouraged by the failure of the mass vaccination program. The Omicron era phenomenon of constant waves of mass reinfection, even during summer, because these viruses utilize an immune response fixated on Wuhan thanks to our own stupidity, also facilitates serotype formation.
Based on the numbers we now have, it really seems that with BA.2.86 we’re sitting in the Goldilocks zone for serotype formation. It’s spreading fast enough to sustain itself, but it’s not spreading so rapidly that it will wipe out the dominant XBB family. This means it will now have to mutate to survive, to ensure the XBB response doesn’t neutralize it.
If you were to assume the two families just don’t interfere with each other, then you’d expect a doubling in the number of annual infections people suffer. That would be bad enough on its own, as that increases the risk of people suffering damage faster than their bodies can repair. If you were to expect something more akin to Dengue, where the infections aid each other, it becomes a catastrophe.
Over the span of a few days we went from most people thinking this new variant would go nowhere, to the UK government apparently being worried enough about it that they’re bringing forward their vaccination program. This led me to realize there’s another point I haven’t properly explained yet.
BA.2.86 came into existence, due to someone who would have been infected for a year and a half. The mutations it has suggests it will be more virulent than older variants. But importantly, the default assumption we have to make about persistent Omicron infections, is that whatever new waves they spark will probably have pre-Omicron level virulence.
The reason is because that’s what you see when you study chronic Omicron infections:
The milder clinical manifestations of Omicron infection relative to pre-Omicron SARS CoV-2 raises the possibility that extensive evolution results in reduced pathogenicity. To test this hypothesis, we quantified induction of cell fusion and cell death in SARS CoV-2 evolved from ancestral virus during long-term infection. Both cell fusion and death were reduced in Omicron BA.1 infection relative to ancestral virus. Evolved virus was isolated at different times during a 6-month infection in an immunosuppressed individual with advanced HIV disease. The virus isolated 16 days post-reported symptom onset induced fusogenicity and cell death at levels similar to BA.1. However, fusogenicity was increased in virus isolated at 6 months post-symptoms to levels intermediate between BA.1 and ancestral SARS-CoV-2. Similarly, infected cell death showed a graded increase from earlier to later isolates. These results may indicate that, at least by the cellular measures used here, evolution in long-term infection does not necessarily attenuate the virus.
The longer it evolved, the better it got at killing cells. After 190 days, it was back to the lethality of the original virus. This is something people don’t enjoy hearing: The Omicron variants are gradually evolving back towards the level of virulence of the pre-Omicron variants.
The big mistake that people make about viruses is to think that they have to evolve to become less virulent once they begin to infect us. There’s fundamentally nothing that requires this.
Smallpox is the most notable example. It only really became deadly during the Renaissance, it spent the medieval era as a mild childhood infection. What changed? Nobody really knows.
Dengue however, is the more immediately relevant example. Because a second infection with a different serotype becomes far deadlier, the spread of people around the world leads to far more people suffering multiple infections by different serotypes of Dengue. This is the main reason it became such a problem since the second world war.
The new BA.2.86 variant clearly is not about to disappear. Rather than directly competing with the XBB family, over the coming months it will evolve to carve out its own niche. That’s its only viable survival strategy. Then we will find out that humanity is faced with at least two simultaneously circulating serotypes.
SARS viruses are intrinsically just very big threats to our species. We know this because we can see that our genes rapidly changed to deal with them in the past thousands of years ago. This happens when they hurt a lot of people.
Our immune systems evolved to arrive at whatever optimal response they can produce to these viruses. When we deploy a poor vaccine against such viruses, as the IgG4 antibody response now clearly beyond any reasonable doubt illustrates we have done, we permanently impoverish our collective immune response towards these viruses.
It would be easy to imagine a conspiracy by radical misanthropic environmentalists as responsible for this. But the reality is probably far more banal: Two superpowers experimenting with viruses to produce a new vaccine for military defense purposes, something going horrifyingly wrong during such an experiment, then a greedy real estate mogul elected president and his incompetent staff pursue a vaccine at “warp speed”, corporate greed leads vaccine developers to push an unsafe solution and rather than question the risks, scientists respond as a monolithic group.
I’m not entirely convinced of van den Bossche’s endgame scenario, because I suspect that a heavily glycosylated Spike protein would not have a survival advantage: Although this would obscure the peptides to which most antibodies bind, the human body also produces antibodies (mostly IgM) that just react to anything covered by a large number of sugar molecules.
Rather, I’m expecting that with multiple simultaneously circulating serotypes, we will just see a rapid deterioration of the situation. One article more or less won’t solve this situation. Rather, I’m honestly just motivated by a morbid curiosity.
I used to think our civilization would eventually collapse due to the changes to our atmosphere, with humans retreating into megacities that block the sun, taking down non-human species with us as the heatwaves gradually just become too severe for above-ground vertebrate lifeforms to survive.
But now it’s starting to look more as if life on Earth can outlive our species: We will descend into a grey haze of dementia and immune dysfunction, unaware of what is happening around us, as the world around us recovers.