AIDS in the intestinal tract: The SARS2 endgame?

An interesting hypothesis from @michaelmina_lab ! Will need to watch other countries WW when Pirola takes over.

Such tropism change would very unlikely occur with HK/HV, but is plasible with such a big evolution to Pirola.https://t.co/CSq4olSrbC

— JWeiland (@JPWeiland) November 21, 2023

Your body has about as many bacterial cells, as it has mammalian cells. How is that possible? Large parts of your body don’t contain a lot of cells. Your bones for example, are mostly just calcium. Your skin is mostly extracellular matrix, proteins like elastin and collagen. Your body is like a bee hive, within which the bees that built it live, rather than being built up of those bees.

When viruses infect us, they can cause persistent infections, which get a lot of opportunity to evolve and produce new radically different mutations. Those radically different new viruses will then be able to fool our immune systems into not recognizing them. An example is BA.2.86. This virus spent more than a year infecting someone, before it had mutated enough to find a version of itself that can spread around the world.

Now my question to you is: Where do you think a virus like this hangs out? Where does it learn to produce a version of itself that can survive for a long time in our body? Our blood is supposed to be sterile. All our cells have an immune system, both an innate system in the cell itself and white blood cells that travel around our body looking for infected cells.

So as a virus that wants to stick around in a human being, where do you go? There are different options to consider. Certain organs normally don’t have immune cells showing up and antibodies should not be able to reach those tissues. The brain and the gonads are examples, they’re protected by a barrier. But another candidate to consider, is to just infect bacterial cells in your gut!

Maybe because there is better persistence in the GI tract?

FCoV also persists in the GI tract of cats, making them permanent walking virus factories.

— Gönndalf ?? (@drallcome) December 11, 2023

That’s probably not easy. To get into the gut, you have to pass the stomach. So you probably need to be able to infect both the epithelial cells in our body, like the endothelial cells lining our blood vessels, as well as our gut bacteria. As our epithelial cells get better and better over time at keeping you out and our other organs get better too, the gut bacteria will increasingly turn into your best available place to survive.

For a virus to survive in our gut, it needs to find the right bacteria. But when it can survive in those bacteria, it will have found itself a very nice place to stay, from where it can constantly jump into the epithelial cells that line our gut. This becomes very taxing to our immune system over time. It would first reveal itself as diarrhea during the acute infection, but you would expect it puts people at risk of Crohn’s disease and inflammatory bowel disease too.

We would expect the virus, as it evolves to become more persistent, to arrive at the molecular sweet spot: The place on the molecular landscape where it can infect both our epithelial cells to enter our bodies and the gut bacteria where it can survive without being eradicated by our immune system.

Why don’t all viruses do this then? Well, other viruses have other tricks in their playbook. HIV is also a chronic infection, but it can achieve this by putting its entire genetic code into our own cell’s DNA. SARS viruses can’t do this. Herpes viruses stick around in our nervous system, but these viruses can avoid eradication there by going dormant and just not drawing attention. The SARS viruses can’t go dormant.

With the whole population now having antibodies against SARS2 that have failed to exterminate the virus, the logical route is for persistent infections to cause waves of new radically divergent variants. Our immunologically privileged organs and our non-mammalian cells are logical places where such a virus would survive. We’ve already seen the variants that aim for the brain. BA.5 was such an example. But by now, it would seem that our brains are on the lookout for this virus too.

Your gut bacteria are different. Your gut bacteria will never remember a viral infection, the way your long-lived brain cells can.

The makeup of your gut microbiome depends almost entirely on the sort of food you eat. They’re all able to digest different kinds of nutrients, the sort of nutrients you eat thus determines the sort of bacteria you end up with. Some of your gut bacteria are going to be better hosts for SARS2 than others.

About two years ago, I explained that SARS2 was going to go through an evolutionary radiation, with many different forms of the virus, specialized in surviving in different methods. You’re likely to witness the birth of bacteriophagal forms of SARS2, that specialize in infecting our gut bacteria.

These versions of SARS2 may exist alongside neurotrophic forms of SARS2, which specialize in infecting our nervous system, as well as alongside respiratory forms of SARS2, which specialize in infecting our respiratory tract. You may even see forms that specialize in infecting our white blood cells.

With JN.1, it seems the virus has arrived at a new version of its Spike protein that is much more competent at infecting cells. It’s now more akin to pre-Omicron lineages again.

There is no obligation for a corona virus to remain one type of disease. In non-human animals, you see corona viruses that evolved to specialize in infecting very different types of tissues. There are corona virus that cause intestinal disease in dogs, pigs and cats.

It’s important to understand that the cat corona viruses that cause intestinal disease are profoundly dangerous. Sometimes these viruses mutate into a form that can infect a cat’s white blood cells. Once this happens, the untreated mortality rate is 100%. These versions of the virus normally seem unable to spread from one cat to another however.

This is a plausible eventual outcome of the failed SARS2 vaccination experiment. We know that this virus persistently infects bats and we can tell that we’re giving birth to variants of this virus that become better and better over time at persistently infecting our own bodies.

We know from cats that a persistent coronavirus infection in the gut can result in a mutation into variants that learn to consistently infect white blood cells in the gut, sacrificing their ability to transmit from one cat to another in the process. These versions preferentially infect monocytes. Without a high pre-existing concentration of monocytes in relevant tissues, you would expect such a virus could not spread into another cat, simply because the virus fails to find sufficient host cells.

But in Cyprus, this feline coronavirus does recently seem to have found a molecular sweet-spot, where these highly lethal white blood cell infecting versions of the virus figured out how to transmit themselves from one cat to another. This is thought to have killed 300,000 cats so far on Cyprus, in just half a year. This is about 20% of the total cat population on Cyprus.

When you have this many individuals infected by a lethal coronavirus, then you’re just not able to treat them all. And this is the problem we’re dealing with. We know SARS2 continues to kill about an order of magnitude more people than influenza every year. But this virus is new, damages the immune system and is nowhere near done with its evolution.

You can look at the concentrations in wastewater, to see this illustrated. Have a look at wastewater in the Netherlands:

We’re now at almost twice the old Omicron peaks, with no end in sight.

I think these three points are important to point out:

1. Most corona diseases we know of in animals are not respiratory infections, but intestinal infections spread through the oral-fecal route. It appears that SARS2 is evolving to function more in the latter manner and less in the prior manner.
2. Persistent corona virus infections in the gut sometimes result in AIDS-like syndromes in animals with a 100% untreated mortality rate.
3. SARS2 is known to infect white blood cells and causes persisting immunological problems in many people.

This virus has only been around for just over three years. Its evolution has accelerated in recent years. There is exactly nobody who can tell you what its end destination is. There is not even someone who can tell you the number of end destinations.

People argue back and forth about the immune system problems caused by SARS2. But there is exactly nobody who knows what happens to human beings, ten years after suffering two infections a year from this virus. And there is exactly nobody who knows how much immune system damage the variants that will be circulating ten years from now cause. But so far, here’s what we see:

I’m curious what 20 lifetime infections after ten years would look like.

I base my own views on what I see. What I see is that concentrations observed in sewage are reaching new record heights around the world. That suggests to me at least some variants are becoming something more akin to an intestinal syndrome.

It may be perfectly possible for hospitals to treat patients against an AIDS-like syndrome from an untreated persistent intestinal SARS2 infection. But keep in mind: The untreated mortality rate for SARS2 is currently less than 1%. If persistent intestinal SARS2 infections result in an immunological syndrome, it will require entirely new treatment and diagnosis options and treating the entire population may be impractical.

And I have to emphasize again: People vaccinated most of the population. This results in an immune response that was once reasonably good at preventing severe disease in the minority of people at risk of severe disease. But the immune response they induce, can not produce sterilizing immunity.

The NK cells are the type of cells that destroy an infected cell very early on during an infection, or help such a cell eliminate the viral RNA. The vaccines were designed to give the task of destroying infected cells to another type of cell: The CD8+ T cells. Those cells can not destroy infected cells early on during the infection and thus they can not provide sterilizing immunity.

By now most people suffer elevated levels of exhausted CD8+ T cells. Not all your CD8+ T cells are exhausted, just the ones able to recognize SARS2. They were assigned a job they’re not intended for and they’re forced to do that job on a constant basis now.

When these vaccine peddlers tell people that the CD8+ T cells can still recognize the virus despite the mutations, you need to ask yourself what that means. It means the virus is under no real pressure to avoid those CD8+ T cells. Why would that be? Because the sort of CD8+ T cells that recognize it are an easy match: They’re exhausted!

The important thing is to ask ourselves, how the virus survives in people’s gut. This would seem to be due to certain types of facilitating bacteria this virus can infect. When we look at what is happening to the cat population on Cyprus now, we should ask what sets cats apart from other animals: Cats are obligate carnivores.

I expect that a plant-based diet will prove to be the best protection against the emerging intestinal variants of SARS2. I’ve already made a bunch of posts on that topic, I’ll avoid excessively repeating myself.