On interferon suppression: Why virulence is now likely to increase again

As I’ve said before, there’s no requirement for the SARS2 virus to evolve to begin behaving like a mild human corona virus that we barely notice. It’s a widely popular myth that viruses must inevitably evolve to become milder because they have to avoid killing their host. Evolution causes viruses to take on whatever form allows them to survive. Whether they become deadlier or less deadly over time is very hard to predict.

For new viruses capable of reinfection, intrinsic virulence can be masked, as more people get reinfected over time and can recall immunity they had already developed. It will seem as if intrinsic virulence has reduced, as almost everyone will have some tools in the toolkit ready for the job. A noticeable exception that makes intrinsic virulence visible may be infants, who were not around the build up immunity to older versions. What you’ve seen over time is that more infants are now being hospitalized with COVID, which is of course an awful thing.

Virulence has to be thought of as a side-effect of a virus pursuing the conditions that allow for its survival over extended periods of time. It’s intuitive to imagine the death of a host would substantially interfere with that, but this is unlikely to be the case when:

-Most transmission happens before severe symptoms emerge.

-The demographic spreading a virus is very different from the demographic dying of it.

-The infection fatality ratio is low to begin with.

All three of these principles apply to SARS2. Finally, as a sidenote, it’s perfectly possible for some viruses to transmit after death, ebola and smallpox are examples of this.

To ask yourself how virulence of SARS2 will evolve it’s more useful to ask yourself: How will this virus have to change its behavior, to enable its persistence in our population? Then you can ask yourself: How would those changes to its behavior affect virulence?

Finally, it’s useful to ask yourself why virulence ever plunged to begin with. The move from Delta to Omicron revealed a sudden dramatic plunge in virulence, evidenced by a sudden wave of infections without an associated substantial spike in deaths in most places. To some degree the plunge in virulence was an illusion brought in by an expansion of the susceptible demographic to include more young people and more people who already had survived an infection, but the reduction in virulence was also a real phenomenon.

The reduction in virulence can be explained through one simple principle: A version of SARS2 that was circulating in rodents jumped back into our species, became known as Omicron and began to spread because its different version of Spike suddenly had a huge transmission advantage in our population. Whatever flaws the virus had for transmission in humans as a result of its time spent in rodents did not weigh up against the massive immune escape advantage it had.

In rodents, SARS2 appears to have a very high fatality rate. Wild SARS2 was found to kill 100% of infected humanized mice, wild SARS2 with the Omicron spike kills 80%, while Omicron itself kills none. So it seems logical to expect there are genes beyond Spike that had to evolve to reduce the extremely high virulence in rodents, so that it could efficiently spread among them.

We also know what some of those mutations probably look like: The virus is relatively competent at suppressing Interferon, which is the equivalent of an alarm bell rang by your cells upon infection by a virus. Viruses that are good at suppressing Interferon tend to be good at spreading up front before the immune system begins to respond.

We know that the Omicron version became less capable compared to Delta of suppressing Interferon due to mutations it incurred. So now we have a pretty decent picture to explain the mystery of a new version of SARS2 suddenly infecting far more people, while killing or severely injuring far fewer than Delta. It’s mainly a combination of three factors:

-Immunity had accumulated in the population.

-A greater share of infections was now among healthy young people.

-The jump of Omicron into rodents required a reduction in virulence for efficient transmission, which was still present once it jumped back into humans.

And it’s mainly that last factor, that is cause for concern. As it spreads in our population, whatever incentive it had to accumulate those mutations is lost again. In fact, what you see lately are a number of reversions to mutations found in the original Omicron versions, back to pre-Omicron variants.

Once Omicron began to evolve in humans again, you could see that Interferon suppression began to increase again. With BA.5 being much better at suppressing Interferon than BA.1 and BA.2. In fact, it seems to have been even better than Delta at it, but it looked pretty similar in Spike to BA.2 and struck in the middle of summer, so it did not have a cataclysmic impact in most places.

Lately, with the new XBB variants you can see that Interferon suppression is increasing again: Different XBB descendants accumulate the same mutations that suppress Interferon.

You can expect there is now a strong incentive to evolve to become better at suppressing Interferon: Until a few months ago, everyone generally had a pretty similar antibody response to SARS2, meaning that any mutation to Spike that works in one person to escape the antibody response would generally work in others. But now, after widely varying vaccination regiments and different patterns of infection with very diverse variants, the antibody response to this virus looks far more diverse than it looked at an earlier stage.

And so the incentives have now shifted: Rather than escaping the antibodies through mutation, you’re better off not getting caught in the act of infecting cells and having those antibodies deployed against you in the first place! A very effective way to do that is by suppressing the Interferon your infected cells produce upon suspecting they are infected by something nasty.

Unfortunately for us humans, viruses that are better at suppressing Interferon tend to be deadlier. SARS2 for example, was much worse initially at suppressing interferon than the original SARS. Mutations to Influenza that help suppress interferon also increase virulence. Mutating a SARS1 gene to reduce interferon suppression reduced virulence.

Viruses tend to run into a problem however, that prevents endlessly improving Interferon suppression: They tend to need a compact code, so genes will often have multiple functions and getting better at Interferon suppression may interfere with other functions. This might be one reason why the hCov viruses have an apparent ceiling to their virulence.

Unfortunately, SARS2 is based on a bat virus. And what sets bats apart from humans? They tolerate viruses of this nature: It’s pretty useful for a defenseless small animal that congregates together in huge numbers in caves to sleep to carry all sorts of deadly viruses: Predators that want to eat them will learn their lesson the hard way. The bats have adaptations to render these viruses relatively safe for them, adaptations we don’t have.

If you suppress Interferon, you’re preventing both the innate and adaptive arms of the immune system from being alerted. There are however aspects of immunity that don’t depend on Interferon. Pathogens like Influenza and SARS2 too, have glycoproteins that they use to enter cells. The NK cells have receptors that resemble the sort of receptors these glycoproteins would normally bind to. This allows the NK cells to recognize cells which are producing these glycoproteins, as they are displayed on the cell’s surface. The NK cells can then destroy those cells, draw other immune cells to the location and produce Interferon themselves.

The adaptive immune response, which was stimulated strongly by vaccination, does strongly depend on interferon however. This makes perfect sense, when you consider that adaptive immunity is the second layer, that comes after innate immunity: The interferon produced by the innate immune system would normally wake up the adaptive forms of immunity.

This is why you wish to see strong trained innate immunity against SARS2 in people. You can expect to see this in India and especially Africa, as well as among the unvaccinated in developed nations.

The problem, as I explained in my previous post as well, is that we have strong reason to believe that we interfered with the training of the innate immune system: Antibodies will bind to these glycoproteins presented on the cell’s surface, preventing the NK cells from doing their job of killing such a cell through binding to the right cytotoxicity receptor, which then allows them to expand. And as the antibody response now shifts to IgG2 and IgG4 in many people, the infected cells may increasingly not get killed at all.

To get them to kill cells and avoid false-positives, it’s generally important that NK cells experience synergistic stimulation of different receptors: It’s like a drone pilot who has a checklist to make sure it’s really “our guy” before someone is drone-bombed. As an example, they also look for patterns associated with damage to a cell, or patterns associated with infection by a pathogen.

The CD8+ T cells, which also kill infected cells for us, don’t seem to bother with this, because they’re being told to kill by other branches of the immune system. And so it seems reasonable to expect that when cells were exposed to Spike mRNA and stealthily fooled into producing only this one single gene, those cells would have stimulated the CD8+ T cells, but not really the NK cells.

The NK cells are harder to understand, because they’re versatile and elegant. And that’s precisely the problem: As they’re not well understood, humans are easily fooled into embarking on dumb experiments that interfere with these NK cells learning to do their job.

To give a metaphor the Americans will perhaps appreciate, it really seems that in a normal situation the NK cells that have taken up residence in tissues that have previously been infected are the immune system’s equivalent of Paul Revere: They’re supposed to be the first ones to notice something’s wrong and the enemy is here again.

Tragically, humanity bet the whole house on the adaptive branches of immunity that are downstream and relatively easy to avoid through improved interferon suppression.

I don’t know of a good solution. Generally speaking vitamin D supplementation stimulates innate immunity over adaptive immunity, zinc helps as well and we have numerous studies showing people with a plant-based diet fare better.


  1. Niacin increases zinc uptake and serum vitamin D. It’s also a protease inhibitor, increases NAD+ which is dramatically drained in SARS infection. There are other precursors to NAD+, but are rate limited. You will never get enough from diet.

  2. Do NK cells also need interferon to start working? If they work without interferon, maybe this would enable NK cell training in vaccinees?
    Or do Abs still have an advantage over NK cells even with interferon suppresion, hence no NK cell training?

    • >Do NK cells also need interferon to start working? If they work without interferon, maybe this would enable NK cell training in vaccinees?

      They don’t need Interferon to detect infected cells.

      The problem is that if they’re not resident in the infected tissues, they won’t see the virus, so it will proliferate for an extended period of time before being addressed. With a high viral load, the virus can exhaust and deplete the NK cells.

      Hence why you would want to see training by less virulent variants before exposure to more virulent variants. That training now seems to be skipped over due to the vaccine induced adaptive immune response.

    • This got caught in the spamfilter and I had to force myself to approve it because that Ethical Skeptic guy is tiresome and takes himself far too seriously.

  3. I have had periodic inflammation with symptoms that other people call Long Covid for more than a year. Never tested, never jabbed FWIW. Then I started 16/8 intermittent fasting three weeks ago or so. I lost about 5 lbs and plateaued, but the various inflammation symptoms went away. Pleasantly surprised, I looked up the effects of intermittent fasting on the immune system. Good things are being said about that, see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9607422/ . Around the web people say that intermittent fasting “resets your immune system”, whatever that means.

  4. NK cells seem to be boosted by Vitamin C, Vitamin E, Carotenoids, Garlic and Selenium: http://www.askdrsears.com/topics/feeding-eating/family-nutrition/foods-to-boost-immunity/foods-that-boost-your-immune-system/

    Interferon production seems to be stimulated by Vitamin C, fermented red gingseng, poria mushroom and probiotics according to drleonardcoldwell.com/2020/03/02/immunity-against-cancer/

    We are all facing a battle here with an evolving bioweapon. The official institutions are useless, they are only trying to sell the failed prophylactic gene therapy pushed by the drug cartels that hijacked our governments. We need to get some crowdsourcing brainpower together on how to fight this evolving virus, without starting panic again.

  5. The virility of the virus has evolved has pretty much followed the pattern of mildly dampened simple harmonic oscillator. It is to be expected to have some fluctuations around baseline virility as the virus explores the parameter space. The virulity will reach its asymptomatic steady state at some point. If one can time it, the best time to get exposed to the virus is to wait for it’s first steep drop in overall virility.

  6. This was harder for me to follow than some of your pieces, but I still really appreciate it.

    I’m seeing elsewhere that infection with ears-cov-2 restructures the chromosomes, thereby “influencing gene expression.” “These altered 3D genome/epigenome structures correlated with transcriptional suppression of interferon response genes by the virus . . .”

    (https://nitter.lacontrevoie.fr/RadCentrism/status/1639077559773327361#m)(the study in Nature cited just came out yesterday)

    So being infected will cause our bodies to have a worse interferon response. At the same time that the virus is looking to get past our interferon defense.

  7. Sars-Cov-2 is a mycobacterium, not a virus (M. avium). H1N1 was M. influenzae. Omicron is a variant of M. influenzae. Montagnier and his collaborators had noticed back in December of 2021 that Omicron did not have its prion domain activated (unlike Delta), and that starting with January 2022, it was beginning to do so (to slowly activate the prion domain). The virulence of Sars-Cov-2 is caused exclusively by the activity of the prion domain (beta sheet prions). In order to hide the astrobiological source of the pathogenic agent, the term “asymptomatic cases” was invented (the R0 of Sars-Cov-2 did not justify at all the spread of D614G worldwide in just two weeks back in march 2020). Omicron was programmed to deactivate its prion domain for some 18-24 months, and then to slowly regain the prion region again (see the CH.1.1 variant with the P681R mutation of Delta). Sars-Cov-2 comes from the Beta Taurids (June-July) and from the Taurids (September-November) meteor showers, that is why we had huge waves in the middle of summer which were otherwise totally unexplained. 1915-1917: worldwide pandemic of “coronavirus”, actually M. avium. 1918: M. avium became M. influenzae. Sars-Cov-2 has 50% common genome with Mers-Cov (variant of M. influenzae), that is why Omicron will activate its prion domain and turn into Coronaflu, just like in 1918. This Coronaflu will be identified as “avian flu”. Montagnier and his collaborators had also seen that Omicron needed a catalyst in order to activate its prion domain, and that was MPV (monkeypox, where poxviridae is also a mycobacterium, a variant of M. leprae). The isomeric version of Sars-Cov-2, coded with Pseudouridine, forced the immune system of the vaccinees to produce isomeric antibodies (of the IgG format, mostly isomeric IgG4 antibodies).

    • I should be going to bed, but instead I have to explain, again, that you don’t know what you’re talking about.

      By the time we are talking about an immune response, any isomerism caused by the modified RNA has been laundered through multiple layers of transcription and recognition. Put simply, THERE ARE NO ISOMERIC ANTIBODIES AS A RESULT OF THE QUACCINES.

      Now you are apparently taking another batch of crazy pills and conflating viruses with mycobacteria. Regardless of the novel coronavirus, and whatever lies we may be told about it, monkeypox is well-known to be an Orthopoxvirus, which is why the smallpox vaccine works against it.

      • You haven’t done your homework on the subject. Isomeric antibodies were discovered in 1994, and isomeric IgG4 abs are a fact of science. Your charade is contradicted by what happened in the fall of 2021: even because the abs were isomeric, the pharma companies were able to claim that the vaccines were “safe and effective”. Let me explain. Delta was caused by two lethal antibodies: REGN10987 and B38 (normal abs). The “vaccine” forced the immune system to release isomeric abs in extremely large quantities (mostly binding) and much less of the normal abs (including the lethal ones described above). This is how they were able to claim that there were “less severe cases” due to the vaccination. But now the vaccinees have these isomeric IgG4 abs in their system.

        From the very start smallpox (poxviridae) was described and thought to be a variant of M. leprae. You seem too sure of the existence of viruses, without having studied the subject matter. As for Sars-Cov-2 being a mycobacterium, Dr. Lawrence Broxmeyer did isolate M. avium in patients with Covid-19 in the spring of 2020.

  8. https://journals.asm.org/doi/10.1128/jvi.00886-22

    The evolution of the myxoma virus after it was released in 1950 to control European rabbits (Oryctolagus cuniculus) in Australia is the canonical example of viral and host adaptation after a pathogen spillover (1–4). By experimentally infecting laboratory rabbits with viral isolates collected over time in the field, evolved changes in the virulence and pathology caused by the virus can be determined (5). Most famously these studies demonstrated the initially highly virulent progenitor (99.8% case fatality rate [CFR] [6]) rapidly evolved into somewhat attenuated viral variants (CFRs 60 to 95%) that came to dominate in the field. Rabbits infected with these variants survived for longer, prolonging the infectious period giving these variants a transmission advantage (7). This remains the textbook example of the evolution of reduced virulence. However, the virus continued to evolve, and we recently reported that Australian viral isolates collected in the 1990s did not present as classical myxomatosis in laboratory rabbits (8). Instead, they induced a novel amyxomatous disease phenotype that was characterized by a highly lethal immune collapse syndrome, consistent with massive immunosuppression. We interpreted this phenotype as an adaptation to overcome evolving resistance in the wild rabbit population (9, 10), a classic example of a biological arms race. Notably, some of these viruses killed laboratory rabbits more quickly than the progenitor strain, but this increase in virulence over the original progenitor is via very different pathway

  9. “But now, after widely varying vaccination regiments and different patterns of infection with very diverse variants, the antibody response to this virus looks far more diverse than it looked at an earlier stage.”

    Is this not kind of good news? Won’t this make it harder for the virus to rip through the population over and over as the ‘immune imprinting’ scenario speculated?

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