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This is off-topic for your current essay, but I would be interested to hear your thoughts on the possible "Red Death scenario" proposed over at Ecosophia:

https://ecosophia.dreamwidth.org/159009.html?thread=22163233#cmt22163233

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If it’s viremia by tolerance, you don’t really need a mutated spike.

If it’s viremia by ADE, that doesn’t imply sudden acquisition of immune cell tropism as far as I can see; just hopping to other ACE-2 receptors. Potentially with same inflammatory pathology (cytokine storm) as “Covid 19” has consisted of all along - “ADE” already being the apparent baseline disease, not a new danger, as I’ve said for a while but still haven’t followed up with better research...

I confess to feeling like the stupid kid in the room whenever reference is casually made to symptoms of illness being the product of immune response. Like, what? I’ve been sick. I know what cellular destruction feels like. So I’m essentially not qualified to comment on a model that proposes “silent destruction” via immunocompromise as I don’t believe in the consensus of reality that underlies the model. In my intuition, if you’re sick you feel sick.

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The mechanism by which the virus could become essentially invisible/invincible to the immune system might vary: tolerance, original antigenic sin, immune cell tropism, etc.

My main question here is more along the lines of immune equilibrium theory. Conventional wisdom says that viruses hijack and destroy cells, or that infected cells are destroyed by the immune system. That is one end of the spectrum of possible outcomes. If the immune system recognizes and eliminates the virus within two weeks, then the virus must replicate sufficiently to transmit to new hosts within that time, which selects for rapid reproduction, tissue damage, and illness.

On the other end of the spectrum is a situation in which the virus achieves immune tolerance/evasion and replicates at low levels (HIV, HPV, HSV-1), or else enters a dormancy phase with later reactivation (EBV, VZV). The dormancy-reactivation pattern typically leads to illness later in life, while the equilibrium pattern can be mostly harmless (HSV-1), or it can lead to carcinogenic persistent inflammation (HPV) or progressive terminal immunodeficiency (HIV), but it doesn't usually cause symptoms of illness - i.e. the infection is asymptomatic until the effects of long-term gradual damage become apparent.

The question here is whether SARS-CoV2 might follow the equilibrium trajectory, which depends on three things: 1) achieving infection beyond the respiratory system, 2) becoming effectively invisible to or tolerated by the immune system, and 3) being sufficiently self-limiting so as to avoid causing massive tissue damage leading to immune activation and/or death.

The Red Death scenario basically proposes that IF SARS-CoV2 could achieve chronic, low-level, asymptomatic infection, then given what we know about spike protein biotoxicity we might expect this to lead to progressive cardiovascular and/or neurological illness and death. I don't have a good way of assessing its likelihood, but to me it sounds like a plausible hypothesis, at the very least worthy of discussion and investigation.

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I suppose I focused too much on the visuals - "walking the dog" etc - than the core proposal.

My default is to picture coronavirus as favoring rapid / aggressive replication, and to picture innate intra- and inter-cellular immunity as setting the bar very high on lower-competence strains during in-host transmission even under immunocompromised conditions.

The result is a baseline "cellular R0" of less than zero, so only high doses can lead to illness - high doses "raise" the cellular R0 by overwhelming innate immune resources. Here is where you want neutralizing antibodies to have already ramped up, to prevent negative outcomes from viremia; but presumably also you've gotten the attention of enough APCs to prompt some updated T Cell motifs, resulting in a step-wise update to immunity. This is a give and take. From 10,000 feet up it still looks like "immunity" / "just a cold," even if from up close it's actually a lot of grey area in terms of T Cell motif inflexibility ("Original...") and/or a bit of spike getting into the blood and minuscule cardio damage that heals under the radar.

There's more than zero room in that model for "low aggression / low-competence" strains to linger after infection - after the cellular R0 is raised by exhausting innate immunity, the "in hose" evolutionary landscape becomes more permissive, even if "transmission" remains a bottleneck that re-selects for aggressive strains. But my guess is that the room is still quite close to zero, and most low aggression strains are going to get suppressed within the host even while cellular immune resources are still in recovery. Thus why "variant factory" immunocomprimised are rare birds, the exception being people who are already seriously unhealthy or pre-primed for inflammatory / ADE response (https://www.nejm.org/doi/10.1056/NEJMc2031364).

Allowing for a non-zero incidence of chronic infection, I think most people are going to operating in the binary between successful innate suppression and fast-onset viremia during symptomatic infection, and most only landing on the latter side if ADE / inflammation are at play.

THAT said, the vaccinated obviously have a lower safety margin for "minuscule cardio damage" if they're walking around at the border of symptomatic inflammation / arrest.

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So I gather you find this scenario unlikely, based on innate immunity making some level of baseline viral persistence unlikely.

The original thread has expanded, and I have added more of my thinking on the topic:

https://ecosophia.dreamwidth.org/159009.html?thread=22163233#cmt22163233

I'm not so sure as you that SARS-CoV2 is a "party-and-run" virus using my terminology from the other thread. From my perspective, part of the reason we call endemic coronavirus infections "colds" is probably because they can persist at low levels and only cause symptoms upon a transient weakening of the immune response - such as can be caused by chilling, stress, lack of sleep, etc. I can easily imagine this virus adopting a "hide and abide" strategy - as I called it - especially if presented with the evolutionary opportunity to do so by a vaccine that induces immune weakness/tolerance and generates a narrow, easily-evaded antibody response.

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I don’t really see the question of constant presence in the respiratory / GI tract too differently - but I think constant environmental replenishment is critical; and environmental replenishment is driven more or as much by rare successfully transmissive viral challenges even during low-spread / off-season periods; certainly so during waves. Without replenishment, a less than 1 “cellular R0” means the virus dries out before overwhelming innate immunity in some cheekily high number of instances e.g. 9999/10000. So “party and run” is a functional abstraction when talking about potential low-aggression or even dormant systemic viral leftovers.

The virus needs to leave 10,000 leftovers. Invoking the “high aggression bottleneck” required to survive and transmit in the first place, I don’t think the window of “low aggression permissibility” during infection creates much likelihood of that much accidental “replication speed drift.” So a true lysogenic cycle is required; otherwise the virus is being asked to pass opposite bottlenecks almost simultaneously.

Chronic bacterial infections are probably a comparable dynamic. You need a really high starting dose directly into the bloodstream, as from a prolonged tick bite, to seed enough low-aggression outliers in enough places throughout the body.

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"So a true lysogenic cycle is required; otherwise the virus is being asked to pass opposite bottlenecks almost simultaneously. "

Like us, this virus has several billion years of evolution behind it, and it carries 29,900 nucleotides of genetic information encoding 29 proteins. I have to imagine that over the course of its history it has probably employed both strategies - "hide and abide" or "party and run" - in order to maximize its chances of survival. Your own Immune Equilibrium theory talks along about dormancy timers and the ways in which viruses switch between lysogeny/rapid replication and dormancy/persistence.

Is there a reason why you don't expect that SARS-CoV2 would be capable of this?

I agree that probably 99.99% of viruses that "land" are destroyed before they can cause infection, but once lysogenic infection is established generating numbers well into the billions, it seems reasonable to assume that some might find a place to hide, and/or that some of the viral genes might function to blunt the immune response in a way that allows for chronic, asymptomatic persistence in some tissues. And it also seems reasonable to assume that our vaccination effort might increase the chances of that happening through several potential mechanisms.

Wound bacteria are largely opportunists; viruses depend on us for their survival. I would be surprised if chronic/long-term infection was not part of that strategy.

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Who among us has not casually, at one time or another, described our kids as “afebrile, active and playful.”? C'mon man.

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Just as long as the Mom understands that her children have a "Temperature" and a "Temperature Identity," and they might not be the same, I see no problem with the term.

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Nov 25, 2021Liked by Brian Mowrey

We humans and our modern ''relationship'' to illness, death and viruses. A sad story, indeed.

Ever read something by Ed Cohen? One of his best works goes as follows:

https://womens-studies.rutgers.edu/images/stories/faculty/15.full.pdf

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I have not. As always I work in awareness of all my thoughts on biology / medicine already having been uncovered before, though my Hobbesian revivalism is probably a new spin. I still haven't even read Illich! I am a page into the Cohen paper and quite enamored.

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Re. note 12, I think you may be misinterpreting the illness-avoidance hypothesis. My read on it is that it is not innate (and so may not be observed in other animals and babies), but rather an adaptation in the evolution of social behavior. People in societies learn best practices for generally reducing transmission, some of which work and some do not. In principle it could have some effect, similar to the innate adaptations that make the smell of rotting corpses and other likely-dangerous things repulsive. If anything, babies and children's innate responses to managing disease transmission may be more likely to spread or contract illnesses / immunize themselves / quickly train their naive immune system: eating snot, eating dirt, putting everything in their mouths, etc. Humans' superior ability to form complex societies and learned behaviors provides enormous potential to develop these kinds of adaptation "in software".

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Thanks for pushing back. I'm sure my understanding of the theory is sketchy since I only know it second-hand, so there's probably a game of telephone effect at work - hence why I limited most of my criticism to the footnotes. Doidge's application was definitely shoddy, regardless of the source material. Maybe one day I will dig deeper. But in your portrayal you already mention some of the contradictions I see from outside - finding things "repulsive" does not improve "immunity" (and lots of adults have very limited "repulsive" sensors); most social rituals encourage contact; etc.

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Repulsion results in avoidance behaviors that don't improve immunity but could still reduce the odds of infection. (If the avoidance actually works in practice - most C19 policies are dubiously effective). I think Doidge has a point that tagging people with "sick" indicia can and does result in avoidance which might be helpful.

Of course the plan falls apart if the tags have no basis in factual likelihood of infection (e.g. if non vaccinated people and vaccinated people have essentially the same very small odds of being contagious, then avoiding non vaxed will not have a positive effect). Or if the avoidance strategies are generally ineffective (e.g. sitting down at a restaurant vs. standing up, or staying masked and 6 feet away in a poorly ventilated room, when the virus is transmitted by aerosol).

So repulsion might still be a potentially useful tool, even if in this situation it is applied in a totally ineffective way.

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Nov 25, 2021Liked by Brian Mowrey

Something to keep in mind as well; up until the magikal Chinese bat soup flu struck, parents and society in America had become literal paranoid delusional about the "safety" of the children.

Dodge ball wasn't allowed to be played because some child might get a bruise. Police were called on parents who let their children go walk to the park alone or ride their bike alone. Helicopter parents cleared a path of all obstacles for their precious. Warning signs about nuts and nut allergies proliferated. Safe spaces were created to cater to hurt feelings. Clocks were removed from schools during tests because they stressed the children too much as they felt "under the gun" from a timed test.

But make your child part of the largest medical experiment in history, via the injection of poorly tested spike-inducing concoctions for which the drug companies have immunity from all harms while earning billions in profits?

wHEre dO wE sIGn uP OuR kIDdzZ??!

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Lucky to have just dodged that bullet-proof vest. As an 80s kid I drowned in a lake, choked on a candy when alone at home (it made its way down the chute after a minute of dissolving), climbed 30 feet up in trees, rode around on the back of a moped, before I was six. But then I got stung by a wasp despite standing perfectly still and turned quite cautious for the next twelve years, though probably not by today's standards.

I would call helicopter parenting and Orphania parallel contradictions. Fear of being an "outsider" / unperson can override objective assessment of reality, but doesn't mean no objective assessment of reality takes place at all. So it's ironic, but still understandable, that risk-averse parents are willing to risk their child's life on an experimental toxin.

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I wonder if the vax liability indemnification applies to misapplication. I'd certainly get a lawyer and find out. Litigation is the most likely road to ending this. adflegal.org is doing some good work, and directly apply donations to that work.

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While I'm too cynical RE the legitimacy of Western governments to agree that litigation is the way out, the idea of a mis-dosing attack is brilliant. Especially as it can easily be argued (because true) that Pfizer guaranteed the mis-dosing hazard by their broken label / diluent scheme.

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Interesting! You are saying many of the same things that I have written (see e.g. http://www.luterra.com/blog/?p=1335), and that I have largely expressed in terms of concepts and language pioneered by John Michael Greer (see his book "After Progress"), and your thoughts with regard to sin and social appeasement echo those of Charles Eisenstein (e.g. https://charleseisenstein.substack.com/p/mob-morality-and-the-unvaxxed).

However you use different language which leads me to conclude that you have come to your conclusions independently, and you single out *rejection of biological death* as the primary underlying phenomenon instead of, say, belief in technological progress, or the sort of psychological mass formation that occurs during times of wider societal crisis and breakdown of social cohesion.

I think you are definitely on to something, thanks for sharing!

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That doesn't surprise me! - though I still haven't gotten to reading it (despite meaning to) I could not help but notice the bold title on your blog. Eisenstein's reminder that the Believers do not care about the "truth" of what they believe definitely influenced the September 1 post that covered a lot of the same ground as this one (footnote 13); here I have restored a bit of "truth" to the belief by aligning it with the set of actions the intuited "Entity" takes on the other / outsider.

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