Die Herd
Note: The history section of this article inaccurately describes “Herd Immunity” of being almost nonexistent in the literature before 1967. It was in fact discussed in the context of flu seasonality in the 50s (https://journals.sagepub.com/doi/pdf/10.1177/014107688607900709). I hope to rewrite this essay at some point, anyway!
Herd immunity to SARS-CoV-2 was never possible. Meanwhile, even expert consensus has declared the “Covid Herd Immunity” myth to be dead. But an autopsy of the myth faces a central obstacle: Does anyone know what the experts meant by it to begin with?
In America, we like solutions.
The Sterilization Fallacy
The second section of this essay will grapple with the thorny nebulousness of what experts actually meant by herd immunity in the context of SARS-CoV-2. Did “herd immunity” mean no more infections with SARS-CoV-2? Rare infections? Continual, common-cold-like infections? Did “herd immunity” rely on Covid vaccine efficacy or not? Did it rely on natural immunity or not? Just what did it mean?! Was Bill Gates personally going to buy us all a goat?! Tell us what it means!
But, for now, let us take it as a given that not all, but many portrayals of the concept hinged heavily on the notion of “sterilizing immunity,” whether induced by the vaccines, or natural post-infection immunity, or a sloppy cocktail of the two. This fallacy will serve as the focal opponent for my Official Theory of Herd Immunity Impossibility, aka Brian’s Immune Equilibrium theory.
I find it impossible to only write out the former in any manner that is compelling; they are bound together. Therefor this essay will use the latter as an introduction to the former, if readers will bear with an introduction to a subject that might not be as apparently relevant to the presently ultra-hot topic of herd immunity.
Additionally, if the whole theory, and Tenet 3 particularly reads like a too-clever thought experiment derived from the most superficial examination of current research possible - well, trust me, it is not. I arrived to the vague outlines of the theory 10 years ago - so, technically, it was derived from the most superficial examination of the then-current research possible. But at the time I was certain that this thing, the idea whose dark outline I had vaguely perceived, would come to dominate research within the next few years - that mankind was on the threshold of a new biological revolution.
And yet ten years later, the revolution has not arrived. It is clear that Science™ is dragging its feet on the matter. However, there has been partial progress. A handful of authors and papers have associated the terms “immunity” and “equilibrium” explicitly in the last ten years.
And something like a hundred researchers have spent the decade delving deeper into the relationship between the microbiome and immune competence. So in a sense I do not claim any authorship of the ideas below.But this essay, importantly, still and only represents my version of the theory. Although I will use the term Immune Equilibrium for the theory, as nothing else is adequate, readers should not take this essay to be a summary of credentialed thought on the term in any manner whatsoever.
Readers will also observe overlaps with the so-called “hygiene hypothesis;” but this theory is derived from a totally different starting point: The modern revelations of how both bacteria and the multicellular immune system coexist with viruses.
Additionally, I offer the reader a list of claims for the performance of this class of theory in explaining observed reality and forming future predictions in the footnotes.
Lastly, some of the tenets of my version of Immune Equilibrium are shared with other sources, but typically only in Tenets 1+2 alone, or in the sub-points of Tenet 3 absent of the core of 3. It is that central point which is the sine qua non of the theory:
Immune Equilibrium, and the Impossibility of Herd Immunity
Immune tolerance of bacteria is the essence of “immunity” from bacteria.
Bacteria are directly and indirectly critical to most or all facets of immune competence.
For viruses, the immune system’s “goal” is to balance host and viral survival. This is why the immune system acts like that is its goal. Antibody levels are meant to drop after a cellular immunity rest period, as a bid for reencounter and re-spread with a given viral challenge.
This strategy removes selection pressure for core immune-evading traits within respiratory and gut viruses, preventing the immune system from having to “solve” the unsolvable in order to ensure basic survival; it additionally removes pressure for antibody escape, slowing the generation of novel antigenic structures in any given virus.
Further:
If a virus happens to take on core immune evasion traits, the fitness gains are either contextual (for rare-frequency spread pathways, immune evasion is probably essential to survival) or short-lived (elimination of host species). The virus must learn to turn off replication and enter lysogeny / dormancy immediately upon access to vital organs, analogous to how bacterial viruses (phages) turn off replication at a certain threshold within a given colony. This explains timed dormancy in common childhood viruses like herpes viruses and hypothetically hepatitis viruses. These viruses are not “defeated” by the immune system - they turn off themselves. Reactivation of dormant, “onboarded” immune-evading viruses is plausibly a reply to tissue stress sensors that indicate a decline in host health.
Dormancy-triggering timers are plausibly calibrated to the immune competence of their host species and may become overclocked over time as a result of artificial immunization (Marek’s Disease herpesvirus, possibly Measles and hepatitis viruses).
For viruses in high-frequency spread pathways (respiratory and gut viruses) without immune-evading traits, there is no evolutionary curve to “more contagious / less deadly.” Novel respiratory viruses without core immune-evading traits merely become another familiar, host-species-sustained virus immediately after first encounter. Contagiousness is thereafter defined by the portion of immune bandwidth a given virus happens to occupy (such as the incredibly versatile ACE-2 receptor pathway). “Deadliness” is thereafter defined by the immune competence of the host population at a given moment. Such respiratory / gut viruses may in fact feature legacy evasion / dormancy genes, but these will be rarely triggered: As stated above, the immune system’s promotion of reencounter and re-spread removes any incentive for these viruses to sabotage cellular immunity.
“Herd immunity” to almost any virus via widespread, persistent “sterilizing immunity” is thus not naturally possible, regardless of animal reservoirs.
An intentionally transient and gradated antibody immunity (humoral immunity) prevents the various flaws of cellular immunity from being exploited. How we coexist with viruses is the same as how we coexist with bacteria: By making peace, not waging war.
Natural adaptive (post-infection) immunity thus both provides a lifelong safeguard against viremia (when viruses escape beyond the infection site, and in excess of what is needed for successful spread) and calibrates for a high likelihood of mildness of reinfection.
This may seem like a let-down, as far as alleged proofs go; less like a rigorous examination of reality, and more like showing up to court in an “Intuition” T-shirt. But to keep the focus of this essay on Herd Immunity, it will have to suffice for now - even if there still remains a universe of other implications to consider.
In the follow-up to this essay, which should post Wednesday, we will examine two of them: The plausible impossibility of functional “biological sterility,” as well as the likely centrality of viruses to both prokaryotic and multicellular long-term survival.
‘Cause half the problem is seeing the problem.
The Three Chiefs
I mentioned, previously, that I find it hard to understand what epidemiologists understand themselves to be doing. In no realm of their “work” is this more the case than that of herd immunity.
But for this and all terms of the field, we must first divide the “meanings” of the term between the parities which are using it.
There is what the lay user means; what the “science journalist” or public-facing official means; and what the expert means; all three are further subjected to the filter of what is compatible with the scriptures of “The Good Book” of medicine, Germ Theory Dogma. At times experts will make gestures or intimations toward recent research which upsets that dogma, and accords with the outline of Immune Equilibrium offered above; however, since they never renounce the dogma, these gestures cannot be used to disqualify other aspects of our picture of what they mean.
Meanwhile for herd immunity, like every other term in medicine, what the lay user means is more or less a sales-pitch fantasy of what experts actually think - with, of course, the interlocutors of “science journalism” obligingly developing and distributing the marketing materials.
The result of this elaborate epistemic polymorphism, is that every tenet of modern medical fallacy is forwarded to us via a distributed motte-and-bailey argument; and while the bailey is often a glossy fantasia of medically-delivered bliss, the motte is inevitably an invincibly dense nest of vague hedges, previously-cited disclaimers, and demurrals to the intrinsic uncertainty of nature, in which the “well, in the end it’s just a theory” cop-out is the ever-incubating egg.
You cannot attack the nest without becoming enmeshed in it; and finding your own arguments yet one more strand that was already part of the construction.
To answer “what do the experts mean by herd immunity to SARS-CoV-2?” is to pull at the strands of this nest, and attempt to pin down the theological superstitions of a furtive and byzantine ministry from outside.
I have merely done my best; the reader is encouraged to be skeptical of my result. Ultimately, my reconstruction of the history of the term consisted primarily of scouring the primary sources cited in papers by Paul Fine from 1993, 1995, and 2011.
The result:Herd immunity in the context of SARS-CoV-2 has been a deliberate fraud from the start. “Herd immunity,” when used by experts:
Has never described “eliminating” SARS-CoV-2 except in the context of worldwide, ~100% adoption of ~100% “sterilizing” vaccination.
Has repeatedly made claims to thresholds for “controlling” SARS-CoV-2 (reducing spread so that “waves” no longer occur) that depend on the dishonest use of the randomized, homogeneous formula that the field of epidemiology established as invalid (or only valid when accompanied by perpetual track-and-tracing for a non-asymptomatically spreading virus) 50 years ago; and has of course done so knowing that the lay public imagined these fabricated thresholds were for eradicating the virus to begin with.
This fraud has been perpetrated knowingly by epidemiological experts and either knowingly or unknowingly by our worse-than-useless expert-interpreters in the press, who should one and all be locked to the stocks in their nearest town square.
While debate has indeed raged on this subject from the first time the phrase was weaponized to sell a vaccine campaign, the only standard that comes close to an orthodox value for “eradicating herd immunity to a respiratory virus” in the field, is worldwide ~100% vaccination with a ~100% “sterilizing” vaccine - and has been so for five decades.
Mind, our threshold for defining fraud - as in intentional deception - relies on the standard-defined rate for effective vaccination: Even if the Covid vaccines stopped infection and spread, which they don’t, every promise made by experts that feasible vaccination rates of 70 or even 80% would lead to their self-defined herd immunity standard would have still been a lie.
Now, let us attempt our historical reconstruction.
The programme seems to have been able to find solutions to most of the problems it faced!
We may regard the term herd immunity as more or less a self-assigned, late-60’s era trade anachronism, roughly as artificial and ahistorical as “country music,” but far more hotly contested within the actual industry.
Upon its arrival, it immediately bore no resemblance to one of the potential first applications, a primitive and limited study on immunized mice in 1923.
Very little use of the term was made in the following four decades, despite the eventual burgeoning of interest in immunizing livestock to protect them from “crowding.”So when the term as we know it today finally emerged in the late 60’s, it immediately became the center of scientific debate over the very meaning of the phrase itself. Only a handful of authors had, before then, explicitly fielded the concepts suddenly being advanced as a new theoretical framework for modern epidemiology; not only was consensus supporting the new framework at that moment utterly impossible, it was almost universally rejected. But “herd immunity” was not, however, at that inceptive moment, a marketing term directed toward the common man: The target market for this first campaign was instead the client’s more powerful counterparts in Congress and at the Department of Health, Education, and Welfare.
And the client and ad team combined, in this case, was the CDC - then still under the umbrella of the Public Health Service.
These three self-interested public health bureau chiefs, alone, are seemingly responsible for the myth recently used to swindle the entire world.
But as they chose to launder their sales-pitch through formal scientific channels, the blowback was firm, in part because their proposition - that measles could possibly be “eradicated” via the novel vaccines then in circulation - flew in the face of prevailing beliefs; and in part because the proposition wasn’t even supported by the CDC chiefs’ own text!
It was, after all, pure bureaucratic sales-pitch, for a product that was known from the start to be complete fiction. The “Theory of Measles Epidemics” offered by the chiefs, in fact, is nothing more than a naked counterfeit of actual scientific argument.
What the chiefs mean by “eradicate” is almost never clearly defined, save for a lone reference to “total disappearance”; their threshold for theoretical “herd immunity” is never pinned down, despite their putatively authoritative assessment of a single, flawed data-analysis from Baltimore which was already three decades old; no mathematical model for defending their theory is offered despite their assertion that to do so would produce a result that is mathematically “simple” (!); how merely vaccinating 1 year-olds is meant to prevent outbreaks or “eradicate” a virus in a country visited by a hundred million tourists a year is never even brought up; and their actual policy prescriptions do not describe “eradication” at all, only a perpetual system of childhood vaccination and outbreak control! (emphasis added):
In fact, it is difficult to estimate whether the threshold of herd immunity for an average American city now would be higher or lower than Hedrich’s [55%] estimate for Baltimore 30 to 70 years ago […]
There is no reason, however, to question the validity of the basic assumption that the occurance of measles epidemics depends upon the balance of immunes and susceptibles,
and that for all areas and special groups in this country the immune threshold is considerably less than 100 percent.Therefore, in a country where smallpox, diphtheria, and poliomyelitis have been brought under effective control through immunization of a moderately high proportion, but by no means all infants and children, so also can measles be controlled with the attainment of immunity levels that are reasonable and wholly practical to achieve. […] the course of measles that will follow a nationwide control program will be comparable to that of smallpox; namely, the total disappearance of the infection promptly when the immunity thresholds have been attained.
And here, again, the CDC chiefs are being evasive. Their subsequent snake-oil plan for “[One-Year] Eradication” restores the requirement of [necessarily perpetual] universal vaccination for young children, thus invalidating any reference to a “threshold” at all, but retains the qualifying reference to “control” (emphasis added):
Essential Conditions for Eradication
With these theoretical considerations, it is now possible to specify the four essential conditions for eradication: (a) routine immunization of infants, (b) immunization of all susceptible children on entry to school or other place of congregation, (c) surveillance, and (d) epidemic control.
So, the phrase was a complete fiction and fraud from the start.
But, because it nonetheless prompted a storm of scientific debate, a more official, orthodox definition for the novel phrase was arrived to only four years later, one that held for the next two decades. We must now discover what that was, and whether it included “eradication” or not.
The push-back to the CDC chiefs’ pseudo-scientific claims was, as said, firm; but in fact not as swift as it might have been. For while epidemiological thought on the (un)likelihood of vanquishing polio virus was, at that time, somewhat ambivalent, the WHO in 1967 had simultaneously rebranded and relaunched their Smallpox Eradication Initiative - and “the science” on smallpox was far from settled.
Here, the available evidence from which to form a prediction was entirely mixed: The vaccinated global north had largely banished the virus by then; while in the unvaccinated global south it still raged; and yet in India - the likely place where modern human smallpox emerged - it raged as well; despite the fact that India had been aggressively vaccinating citizens for smallpox for 100 years by then.
By itself, the CDC chiefs’ assertion of a one-year “eradication” of measles was not even supported by their own text. But in conjunction with a possible against-the-odds victory against smallpox, the impulse not to get caught on the wrong side of scientific history must have been strong, especially on such a rapidly-evolving subject as vaccines - and, in fact, bets against the eradication of smallpox did go on to lose.
Thus, with the conventional wisdom under attack by two grand experiments at once, the definitive refutation of the association between “herd immunity” and “eradication” did not arrive until after the CDC’s measles campaign revealed itself to be an utter failure - a mere three years in.
Despite federal funding, the rate of measles vaccination for American children under the age of 5 never exceeded 70%, about where it was when the campaign launched - whereas the chiefs’ prescription had called for universal coverage. Recorded incidences of measles meanwhile were by no means “eradicated,” if they ever decreased at all. And, as measles had already ceased to drive infant mortality before the vaccine even arrived, federal funding for vaccination was immediately switched to a more politically relevant viral threat immediately upon authorization of the new rubella vaccine, in 1969. Whereas measles eradication was essentially a vanity project with no public support; rubella was the super-threat that had mysteriously caused tens of thousands of birth defects during an outbreak beginning in 1964. Measles cases thus went on to peak at triple the 1968 count two years after the end of the program, in 1971.
In that same year, what would become the orthodox stance on the possibility of “eradicating herd immunity” against a respiratory virus arrived, in the form of a paper by John Fox et al.
In this paper, the simplistic, “random, homogenous spread” model which would later be ossified as the formula “Vc=(1− 1/R0)/E” is attacked by the concept of heterogenous spread.
The authors, via attempting to model a reality which essentially amounted to quantifying how many times the “unlikely” event of two people with a first name starting with the letter I being on a bus at the same time somewhere happens on a given day, achieve the obvious result that it will never be zero.
Thus, a respiratory virus cannot be “eradicated” until there are virtually no infection-susceptible individuals in a population at all.No matter how large the proportion of immunes in the total population, if some pockets of the community, such as low economic neighborhoods, contain a large enough number of susceptibles among whom contacts are frequent, the epidemic potential in these neighborhoods will remain high.... Success of a systematic immunization program requires knowledge of the age and subgroup distribution of the susceptibles and maximum effort to reduce their concentration throughout the community, rather than aiming to reach any specified overall proportion of the population.
And, of course, that’s not even taking into account the rest of the world!
What Fox achieves, by this result, is an outright refutation of the association between “eradication” and “herd immunity,” a refutation which has not been disputed in epidemiology since. Fox affirms, instead, only the definition for the term that he finds in a contemporary medical textbook (emphasis added):
the resistance of a group to attack by a disease to which a large proportion of its members are immune, thus lessening the likelihood of a patient with a disease coming into contact with a susceptible individual
Fox’s clarification appears to have elicited consensus, which pervaded for several years afterward.
Thus, four years after it was laundered through the scientific literature, both the snake-oil double-speak definitions of herd immunity forwarded in the CDC chiefs’ fraudulent sales-pitch were dead. The phrase did not mean eradicating a virus, or even preventing outbreaks. It only meant, essentially, a population “having less infections given moment than they otherwise might.” A novel meaning for an old but neglected term had been proposed, debated, and rejected as being counter-productive to sound policy recommendations.Yet by the 90s, those other two definitions had been resurrected; the debate had only grown more intense; and the motte and bailey fallacy of what herd immunity means had become entrenched and internalized within epidemiology, well before it was ever unleashed on the public via media intermediaries to demonize vaccine choice advocates.
What had triggered this bizarre regression from sanity into fabulism?
The success of the WHO smallpox campaign, of course.
So if there's no expert dealing with the problem
It's really actually twice the problem
Only an Expert
Professor Fine’s first overview of the history of the phrase, in 1993, essentially concedes that Fox’s limited definition had already been overturned, and that the impetus for this reversal was the eradication of smallpox.
Yet this nuanced overview of the “revived debate” does nothing to resolve the contradiction between the suddenly common definition of the phrase - the moment when an outbreak begins to reverse - and Fox’s demonstration that such a reversal has nothing to do with eliminating a disease. And that the two were linked is inarguable. Despite the lack of self-awareness among the scientists engaging in the “debate” which persists until this day, the obvious question has to be asked:
Why would it be interesting to calculate when an “outbreak” of a virus ends, if that doesn’t result in the disease going away for good?
What possible need would man have for that information; for mathematically modeling what was already observable by anyone with eyes, and even acknowledged by the CDC chiefs in the introduction to their presentation 25 years prior?
[Measles] occurs ubiquitously throughout the world in periodic cycles of considerable regularity.
The answer, is that wouldn’t be, and there was no need.
But the suggestion that “transient outbreak reversal” was ever really what epidemiologists have been obsessing over and “debating” since the eradication of smallpox is just farcical. If that had ever been the case, then transient would have been explicitly attached to the term in question!
The field is a disgrace to itself. A festering swamp of magical-thinking zealots in denial, perpetually self-censoring to maintain a fiction of rationality as they pursue an ever-fading frontier of glory while pretending to remain grounded in place. As regards all the manifestations of “corroborating evidence” for the fiction - the fabricated-from-nowhere pseudo-obsession over flattening the curve, to save the “health system” from being “overwhelmed”
- these are the desperate gestures of a reeling addict who has lost every last scrap of concern for whether his own lies are even believed anymore. A drawer-full of receipts for evening drive-through coffee runs, as if buying a coffee every night proves the trash can out back isn’t full of empty bottles.And lest one think that the fantasy itself was ever defensible - that in the wake of the smallpox victory, it was reasonable to “just question” the impossibility of eradicating other diseases again - the fact was that in every other front of the “battle” against viral infection, signals for the efficacy of all vaccines were only worse in the early 90s than they had been when the CDC chiefs made their presentation 25 years prior.
In fact the Measles Eradication campaign had itself been revived twice by that time, thus achieving a resounding, real world triple-refutation of “threshold-based eradication.” In the first revival, from 1971-78, vaccination rates for children under 5 still refused to increase, and case rates were not lowered at all. What’s more, the “gains” of the initial, post-approval roll-out of the vaccine were all suddenly coming undone. The children who had gone unvaccinated after 1963 were now themselves the ones getting sick - even though they were now teenagers:
Unlike measles in the prevaccine era, which primarily affected preschool and young school-aged children, a substantial proportion of cases in the mid- to late 1970s occurred in middle or high school students. In 1977, 82% of reported cases occurred in people 5–19 years of age. Because the vaccination program had reduced the overall incidence of measles, many unimmunized children escaped measles and remained susceptible as they entered school.
All the “herd protection” conferred by the vaccinated to these “free riders” was only an illusion - in fact, it was their peers who, by being force-dosed by their parents with a vaccine whose long-term effects were still unknowable, had prevented them from encountering the virus on a normal schedule. The virus, which had ceased to even represent a threat to children years before the vaccine was released, still reached everyone in the end. All viruses do.
The third campaign, from 1978 to 1988 and supplemented with the most aggressive school requirement push yet, was likewise a failure. And as it took place against a backdrop of the recently-emptied teen “susceptibles” pool slowly rebuilding, case rates only increased, so that in the early 90s they were almost exactly where they had been in 1967. Finally and exclusively, the expansion of legal coercion and the doubling of the doses children were subjected to produced an effect. But even then the virus was not truly eradicated, and the promise of 1967 remained completely unfulfilled. From Hinman, A. et al.:
Similar signs of stalled progress had been observed among every other novel vaccine, besides polio - whose day in court was yet to come. Smallpox was the exception, not the rule. And the fact that it was and always would be an exception was already accepted as fact, by none other than the director of the WHO’s astonishingly successful eradication campaign himself: Donald A. Henderson.
From his 1987 World Health Forum interview:
Does the experience gained in eradicating smallpox set the stage for the eradication of other diseases through immunization?
Unfortunately not. The smallpox eradication programme cannot serve as a model for other disease control or eradication campaigns. Every disease has its own epidemiological characteristics and requires specific strategies for its control. Also the approaches taken to the eradication of smallpox differed considerably from country to country and were continually modified to capitalize on an evolving understanding of smallpox epidemiology and to deal with different local conditions. During recent years, four diseases have been seriously advanced as candidates for global eradication within the foreseeable future: poliomyelitis, measles, dracunculiasis, and yaws. […]
In my opinion, however, the present prospects for the global eradication of most human diseases are not good. Epidemiological characteristics preclude many from consideration, while the nature and cost of available technologies rule out others.
Of the four diseases you mention, which would be the first one that might be eradicated from a continent - or globally?
The feasibility of eradicating poliomyelitis appears greater than that of the others, as poliomyelitis is more universally accepted as being of sufficient importance to warrant an eradication programme […] and good protection is usually provided by both the inactivated vaccine and the attenuated live vaccine.
Nonetheless, Henderson’s younger peers were already committed to the fiction that they would one day follow in his footsteps.
“Herd immunity” was, by the early 90s, merely a euphemism for what these younger experts were hoping to accomplish throughout their entire careers, and alike what they have hoped to achieve by promoting the Covid vaccines to us this year - what they knowingly implied they would deliver to the fellow humans they have simultaneously oppressed: Eradication.
In a sense, this history has in fact exonerated the three CDC chiefs who innovated the Herd Immunity Fraud model. By 1971, epidemiology had already purged the deceptive versions of the definition from the consensus of the field. And like the still near-mythical “eradicated virus,” there was no reason for the fraud to be resurrected twenty years later. It was a conscious, if crowdsourced choice, made by the chiefs’ intellectual progeny, to revive the fraud and use it to blind both the lay public and themselves within a double-speak, forbidden-fruit fantasy of medical deliverance.
Yet if the chiefs have thus been relieved of their share of condemnation, it is not because they deserve to be. The measles campaigns eventually created enough political angst to spur the coercion of hundred of thousands of children into a vaccination regime that the chiefs admitted at the outset no children needed.
This admission, incredibly, appears right in the introduction of their 1967 paper.
In this portion, the chiefs actually succeed in constructing a scientific text that is worth permanent preservation; as a document of man’s modern descent into paranoia and insanity. In fact it reads like nothing so much as the contrived, heavy-handed opening scene of a movie about a novel and unnecessary technological “advance” that leads to existential disaster.
INT. CONVENTION CENTER AUDITORIUM - DAY
For centuries the measles virus has maintained a remarkably stable ecological relationship with man. The clinical disease is a characteristic syndrome of notable constancy and only moderate severity. Complications are infrequent, and, with adequate medical care, fatality is rare. Susceptibility to the disease after the waning of maternal immunity is universal; immunity following recovery is solid and lifelong in duration.
The infection spreads by direct contact from person to person and by the airborne route among susceptibles congregated in enclosed spaces. The disease occurs ubiquitously throughout the world in periodic cycles of considerable regularity. With the exception of a few extremely isolated population groups, essentially all children experience the infection sometime before adolescence. The reservoir of infection is man himself. No nonhuman sources of infection are known. Chronic carriers do not exist.
Despite the extent of the epidemiologic knowledge of measles, health officials have been frustrated in their efforts to bring this disease under control. During the past 50 years the doctrine has become widely accepted in health circles that since control measures have failed, man should learn to adapt himself to the measles virus. Thus, by judicious use of immune globulin for modification of the disease among exposed young children at great risk, and by providing adequate medical care to all patients, the damaging effects of the disease could be mitigated. Until very recently, this deep respect for the biological balance of the human race with the measles virus had become accepted doctrine. Eradication was not considered to be scientifically tenable.
All of this has now changed. With the isolation of the measles virus and the development and extensive field testing of of several potent and effective vaccines [in 1963], the tools are at hand to eradicate the infection.
With the general application of these tools during the coming months, eradication can be achieved in this country in the year 1967.
So when experts say, "Let's get to the root of the problem
Let's take control of the problem
So if you take control of the problem you can solve the problem."
Now often this doesn't work at all because the situation is completely out of control
Anderson, L. (2010). Only an Expert. On Homeland. Nonesuch/Elektra Records.
This journal uses the common definition of “theory” - any set of ideas offered to explain an observed reality - and rejects the trade definition.
Excluding in the context of the modes of cancer.
Perhaps the boldest and most prominent pioneer in Immune Equilibrium theory has been Karin Mölling. See: (2013.) “What contemporary viruses tell us about evolution: a personal view.” Archives of Virology.
Viruses helped in building genomes and are driving evolution. Viruses and bacteria belong to the human body and our environment as a well-balanced ecosystem. Only in unbalanced situations do viruses cause infectious diseases or cancer.
Immune Equilibrium is elaborated here:
Relative to germ theory, a microbiome and virome-inclusive Immune Equilibrium theory:
Is equally adequate for explaining:
Individual/regional immune naivety (as in, why novel immune challenges are highly host-destructive and, on a population level, observable as plagues).
Symptomatic immune challenges as an imperfect proxy for immune familiarity (as in, the general wisdom that if you get sick from a particular viral challenge, you are less likely to get sick from it again).
Evolutionary leaps - if you’re into that sort of thing (as in, horizontal gene transfer from viruses).
Myriad diverse physical and personality characteristics currently attributed to genetics (as in, high prevalence of mental illnesses-like behaviors in all animals; why, for example, in nearly any small grouping of flies, there will be at least one that is much less likely to remain still than the others).
Better explains:
Animal husbandry-induced immune naivety (as in, why artificially limited populations become immune-incompetent to “wild” viral challenges, and why it might be feasible to prevent immune competence without veterinary vaccination).
Why pandemics don’t occur more often in the modern world, despite the constant false alarms (continual international travel offsets for unprecedented levels of locally divergent antigenic drift (good thing we didn’t just shut down international travel for over a year…)).
General divergence in immune challenge event outcomes and overlay with individual health (here Immune Equilibrium subsumes host theory).
Aberrant divergent outcomes (as in, immune-challenge-induced auto-immune disorders; which are so poorly explained by germ theory that we have created 10,000 names for the same obvious dysfunction, the latest of which of course being “long Covid”)
The apparent prevalence of potential virus-delivered evolutionary leaps (as in, the prevalence of endogenous retroviral genomes; this becomes a feature, not a bug).
Stress as a viral affinity enhancer (i.e. immunosuppressant) in both prokaryotic and multicellular organisms. (To be further addressed in the next essay.)
Asymptomatic / Test-confirmed Asymptomatic or Symptomatic immune challenges as a seemingly better proxy for immune familiarity. (i.e., even if you don’t get sick from something, a viral challenge that produces a testable result may indicate lower likelihood of getting sick from that same viral challenge later).
“Waves” of respiratory viral spread. In an Immune Equilibrium framework, individual antibody-immunity to respiratory viral challenge is heightened after a prior challenge, plausibly to provide a cellular immunity rest period, and then intentionally fades. The resultant model for population-wide immunity is one in which respiratory viruses not only can never be extinguished but are burning a fuel that is constantly increasing in potency, until the tipping-point which we call “R0” is crossed. However, although the fuel is now potent enough to combust, it is still an impure and randomly sorted fuel.
This model implies that random luck will determine how long the resulting fire will take to reach viral critical mass and that, once again, the constant potency-creep of the fuel will create an inverse relationship between pre-critical mass speed and eventual volume (as well as with post-critical mass speed; i.e. social distancing only increases the overall amount of spread in a give wave, though this is plausibly a less strong relationship). This further implies that a seasonally-imposed increase in the potency of the fuel - via degradation of the respiratory microbiome from cold air, as proposed below - leads to wave seasonality; both biannual and tri-annual regional wave patterns match this model.
Because Immune Equilibrium does not grant that there is an “evolutionary advantage” for respiratory viruses to slow reproduction (because there is also no advantage for respiratory viruses to evade immunity, because the immune system intentionally supports spread), all differences in respiratory viral spread rates are purely a feature of the facet of immune bandwidth in which they happen to operate.
This implies that the built-in risk of injurious or fatal viremia is either not significant or is a worthwhile fitness tradeoff. I consider it likely not significant, as evinced by the frequent recycling of endocytosis-promoting receptor proteins between epithelium and the cardiovascular and neurological system. As it is, these receptors are arguably all-but designed to facilitate viral replication and spread (a.k.a cellular takeover) - with, once again, possible intracellular firewalls to opening the receptor-mediated vesicle without verifying contents ignored or reserved for immune cells (because, once again, all such firewalls would be overcome if they were robustly employed in regular cells) - and so almost every receptor-mediated portion of the immune bandwidth constitutes a fast-moving game of plinko with the bloodstream and the brain on the other end. This suggests that reinfections with severe outcomes are only possible as a result of extreme rare chance or general (core) immune incompetence.
The microbiome at large:
All traditional digestive tract bacterial monoculture disorders (Cholera, salmonella, C. diff etc.) (as in, why it is often trivial to have a normal background presence in the gut and elsewhere, and why crowding and “incomplete sanitation” lead to drinking water toxicity).
All respiratory and skin bacterial monoculture disorders (tuberculosis, staff, etc.) (as in, why it is trivial to have a normal background presence of “pathogenic” bacterial strains in the respiratory tract and skin and why industrialization and hospitalization leads to illness - sterilizing urban pollutants or hygiene regimes which plausibly either, prompt respiratory or skin dysbiosis directly, or, eliminate live bacteria from the air so that endospores outcompete non-endospore-forming bacteria within the respiratory microbiome).
Urinary tract bacterial monoculture disorders (aka UTIs); stomach bacterial monoculture disorders (the great H. pylori controversy, including the observation that stomach biomes without H. pylori are more diverse - see Section 4 of Alarcón, T et. al. (2017.) “Impact of the Microbiota and Gastric Disease Development by Helicobacter pylori.” - though some small studies have found the opposite) (as in, why more delicate microbiomes may be more difficult to restore after antibiotic disruption, leading to recurrent disorder).
Relationship of microbiome to viral challenge immune competence:
Winter seasonal illnesses (respiratory microbiome degradation from cold weather, leading to reduced pathway interference for viruses via broad-spectrum peptide noise).
Polio (as in, the late-40s surge in severe outcomes: gut microbiome destruction (dysbiosis) / immune dysregulation from penicillin (see below) - although studies in lab mice have shown polio and other enteric viruses to exploit gut bacterial factors (indeed, evolutionary logic would declare that many must do so, as a basic feature of replicative competence), causing antibiotic-primed gene-edited immunodeficient mice to fare better to challenge with polio - see Kuss, S. et al. (2011.) “Intestinal microbiota promote enteric virus replication and systemic pathogenesis.” - so, future research may refute any link between penicillin and polio, but I am skeptical).
Immune “dark matter” (as in, individual / regional microbiome diversity as an explanation for divergent susceptibility to circulating viruses, either via viral exploitation of bacterial peptides or via bacterial peptide disruption of viral binding).
Efficacy of bacterial-peptide-derived (ivermectin) or potentially homologous (hydroxychloroquine) anti-parasitic molecules as pro-immune-regulation therapeutics effective during viral challenge; potential for viruses to develop strategies to hijack any given molecule for eventual improved binding; potential for said viruses to then be disabled by absence of same; various other dizzying ominous implications. Additionally, potential efficacy of antibiotics to inhibit viral function in the same manner; though almost certainly at a net-loss.
Immune “dark matter” 2 (as in, potential for divergent efficacy of such therapeutics by region / season).
The sinuses (as in, why we have them: expanded air-exposed surface area to increase bacterial immune mediation (more priming accelerates immune response to respiratory viral challenge before significant lower-lung / viremia can occur); i.e. a built-in immune biolab (though gut bacteria may actually predominately perform this primer-assist function during respiratory viral challenge - see Winkler, E. below)); and/or to modulate against respiratory biome disruption).
Further reading:
“The Last Microbiome,” from The War on Pee.
Robinson, C. Pfeiffer, J. (2014.) “Viruses and the Microbiota.”
Winkler, E. Thackray, L. (2019.) “A long-distance relationship: the commensal gut microbiota and systemic viruses.”
Immune disorder at large:
Autoimmune disorders, including leukemia, and allergies (aka the “hygiene hypothesis”) (reduced immune challenge and disruption of microbiome immune-mediation both plausibly lead to reduced immune competence).
Immune Equilibrium subsumes the hygiene hypothesis into a framework that sees the immune system’s job as a four-part balancing act: Balancing host and viral survival, and balancing tolerance and destruction for both host and viral entities. The result of this simplistic framework is an even more simplistic model that portrays severe infection outcomes and cancer as essentially the same immune failure - “did not prevent [excessive] spread” - and implicitly removes culpability from most viruses; this is especially relevant for how we think about outcomes to childhood infections (removing any one virus from the world does not enhance individual immune competence and probably does not reduce eventual negative outcomes from childhood illness). Additionally, this model implies that reduced competence in allowing for the spread of viruses - such as would result from insufficient encounter with viral challenge - plausibly leads to reduced competence in self-tolerance. The pattern recognition machine, not encountering sufficient valid matches for “not self,” incorrectly plots signals from “self” into the empty category. So, protecting children from illness plausibly increases autoimmune dysfunction, for a net even or negative result.
The end result of this simplistic framework is that investigations into the mechanism of the immune system become uninteresting from a medical perspective. If it is a pattern-recognition machine, the solution to every dysfunction is to show it more signal, including by vigorous circulation of lymph. Get outside. Work up a sweat. Etc. It must be mentioned that this, for all its stubborn Luddism, is the very same intuitive logic by which vaccines are sold to the clever Western school-children who grow up to regard them as “medical miracles.” Only, no one mentions that injection into the bloodstream is not how almost any natural infections occur, and so most vaccines are not actually showing the pattern recognition machine “the pattern.”
Various aspects of aging (as in, reduced immune challenge from behavioral changes, reduced exercise and contact etc. plausibly contribute as much to reduced immune competence as aging itself).
Provisionally less-well explains, or leaves open-ended:
The successful eradication of smallpox. Smallpox gains a plausible exception to the “Herd immunity is not naturally possible per the Immune Equilibrium definition of immune competence” paradigm due to its unique habit of displaying visible symptoms in advance of possible spread (in fact, the vaccine itself, an already over 100-years old mutant horsepox whose development methodology had been lost to history, was plausibly irrelevant to smallpox’s mysterious disappearance; and even the official account of the Eradication Program is that vaccination, being insufficient on its own, had to be supplemented with track-and-trace programs in every region).
Many self-sabotaging immune behaviors:
Lethargy during illness, which seems to contribute to immune competence spiral (post-immune-challenge autoimmune disorders, which themselves result in lethargy!); though, this is plausibly explained by via other evolutionary-logical routes (limited calorie-access in the wild, and default necessity of resumption of activity after recovery).
Anaphylaxis.
Lentiviruses and filoviruses. As in, the apparent implausibility of pinocytosis as a novel immune-evasion mechanism appearing only in the last five decades of evolutionary history, and subsequent dubious characterization of modern “doomsday” viral “novelties” (Ebola, Marburgvirus, and HIV) as being immune-evaders to any significant extent, rather than scapegoats for iatrogenic immune dysregulation of some type. “Pinocytosis” refers, primarily, to the exploitation of non-specialized cellular lipid transfer pumps for host cell entry. The proposition that such a fundamental cellular entry pathway would only begin to be exploited by viruses circa 1975, resulting in unprecedented immune dysfunction, is, to put it politely, “intriguing.”
Influenza (as in; why does influenza variate antigen patterns so quickly even though it would survive just as well without doing so? Indeed, Immune Equilibrium implies that influenza must also behave as it does as the result of human interventions of some type).
Some types of bacteria that still seem predominately pathogenic under the traditional invader/parasite paradigms (excluding “toxin”-producing strains, as such molecules are usually just biological friendly fire), such as spirochaete. However, a tendency for healthy microbiomes to blunt pathogenicity, or a role for spirochaete in healthy microbiomes might be discovered.
Antibiotic Resistance Apocalypse imminence. Immune Equilibrium predicts that this will not come to pass. Antibiotics should continue to have a productive, but more limited role in effective health care, ideally used as a last line of defense or in conjunction with novel “microbiome restoration” follow-up therapies (microbiome restoration should make residual biofilms clinically irrelevant in the Immune Equilibrium model), and hopefully tempered with an understanding of collateral microbiome damage.
(defunct footnote)
Thus, all attempts to “vaccinate cancer away” are hogwash. The virus only appears because the host tissue is distressed to begin with. Here, as elsewhere, Immune Equilibrium subsumes Host Theory.
Tenet 3-1 provisionally does not apply to rare-spread pathways, namely cross-species injection-based viral infection such as Dengue virus, which seems to produce a semi-nonfunctional immune response.
It does provisionally apply to Ebola virus, which does not seem to have any core immune-evasion features and therefor is likely already a common asymptomatic virus in some if not most of the world. Not only has Ebola virus infection been found to be asymptomatic in fruit bats (the imagined natural host), but dogs. Despite the horrific, death-machine appearance of Ebola virus’s envelope structure, it does not appear to be efficient at entering cells: The observed mechanism of entry is pinocytosis, which is not keyed to any host-specific receptor. Hence it is plausible that all sorts of animals are carriers, if not literally all animals, and that pinocytosis-based viruses are the least novel of animal viruses currently in circulation. This renders it unlikely that pinocytosis proffers any immune evasion advantage, except that which derives from the baseline harmlessness of viruses that utilize this pathway.
I mean if you don’t think the 2013–2016 West Africa outbreak was the result of an undisclosed WHO-promoted experimental Ebola/Marburgvirus/HIV vaccine-induced antibody dependent enhancement debacle at this point, you’re probably crazy!
(defunct footnote)
This refers to the gradual rate of antibody fadeout, which plausibly modulates subsequent viral challenges so that re-infection and spread occur at a lower cost in terms of symptoms and taxation of cellular immunity metabolic resources.
This does not apply to Covid vaccine-induced immunity, which only programs a defense against viremia and seemingly confers almost no immune competency against infection in the respiratory tract. See “Boostermania.”
This additionally does not imply that high viral-load events will not routinely lead to more moderate reinfection outcomes. The plausible long-term outcome is a sort of homeostasis between immune competence and immune challenge, regardless.
Additional implications will be addressed in the follow-up essay.
(Anderson, L. )
We saw this with the acknowledgement of the drop in infection efficacy in July: The experts were able to assert at go that they had disclaimed the possibility (in their argument that the Covid vaccines are nonetheless recommended for all of humanity) all along; the science journalists are already hard at work inventing new, incoherent pro-nonfunctional-vax sales-pitches - “mucosal immunity,” an exciting and exploding realm of research that actually explains the mechanism for therapeutics to viral infection, a points to a possible future where viruses can be rendered benign despite modern poor health - and yet as we speak is being crafted into another fable buttressing the crumbling narrative alter of vaccines.
But, I had never heard it described this way before a day ago, as it essentially functions as a synonym for what I would characterize as “microbiome immune regulation.” For although the term “mucosal immunity” seems to suggest “nasal airway immunity,” it is just as applicable everywhere mucus is produced - the digestive tract, the urinary tract, the eyes, etc. - all places where (species-native) microbiota contribute to functional immune regulation, if only by providing sentinel cells with some form of constant signal-calibration (for an intuitive example, if background toll-receptor engagement is low, it may be difficult for an antigen presenting cell to associate a viral antigen with aberrant decrease or non-increase in toll-receptor signal, thus leading to poor regulation of early IgM generation); additionally, the upper respiratory tract is often quite relatively dry, and yet just as rich with life. So: “microbiome immune regulation,” or “microbiome mediated immunity.”
Discovery of “mucosal immunity,” in fact, seemingly was derived by observations that Salk’s injection-based polio vaccine stopped viral congress to the bloodstream and nervous system, but not symptomatic infection within the gut itself - exactly where we are today with the half-failed Covid vaccines. Meanwhile, neither did the subsequent oral polio vaccine appear to extinguish asymptomatic spread. In fact, were it to have done so, we would expect polio virus to have achieved antibody escape by now (which would be observable in testing of AFM patients who were not being protected by the six decades out-of-date vaccine). The near certainty that we are all still routinely spreading polio virus makes one sound like a conspiracy theorist today, but was still openly debated as of 1993, merely a year before the CDC ludicrously declared the Americas to have “certifiably eradicated” it - see: Fine, P. (1993.) “Herd Immunity: History, Theory, Practice.” Epidemiol Reviews. This pattern of a Mission Accomplished announcement dissonantly blaring overtop inquiries into the efficacy of polio vaccines would be repeated two decades later in India, though the WHO link offered by Wikipedia for the 2017 declaration of “three years polio free” for India have been taken down.
By the way, it has been obvious since the discovery of the role of bacteria in microbiome immune regulation that the surge in severe cases in Polio, a once statistically-trivial gut virus which can only cause severe illness as a result of immune incompetence, was triggered by the mass production of penicillin in 1944. Antibiotics temporarily turn off microbiome immune regulation, leading to paralyzed white American kids (who, of course, were already living in hyper-sterilized, microbiome-disrupting environments to begin with). Oops.
Since few online sources offer a lot of info on US case rates before the vaccine, I refer often to the University of Oregon Mapping History polio chart, as it lumps “permanently affected” and fatal cases together - unfortunately, the source for their figures is not provided:
Additionally we should find it no surprise that “polio-like” myelitis is now on the rise - any gut virus potentially able to take advantage of the same microbiome dysregulation. I may follow up with the Penicillin/Polio theory in a future essay, if I get around to finding a better primary source of case rates. For now I have placed it here so that I can write more directly about the polio, tetanus, and perhaps smallpox vaccines - the holy trinity of our “modern literal life-giving God” - themselves, in a different future essay.
Back to the original tangent of this footnote: In general, I favor applying the broadest possible perspective when thinking about the immune system. It is a pattern recognition machine: It responds in accordance to what is actually happening within the body, not according to any single isolated rule-set within the four billion pathways that make up the biomolecular algorithm. As the Noble Prize-checkmarked expert explaining the evaporation of infection efficacy to his fellow Australians admonished, “it’s hard to keep those antibodies up in the nose” with a shoulder-injected mRNA script that doesn’t even induce actual viral infection. So, as regards using IgA “mucosal immunity” measurements as a surrogate for common sense, I am ambivalent - but given that it has to be, at least, a better method of vaccine-induced immunity tea-leaf-reading than endless blood draws, one has to wonder why it apparently hasn’t been done during the Covid vaccine mass experiment at all.
Fine, P. et al. (2011.) ““Herd Immunity”: A Rough Guide.” Clinical Infectious Diseases, Volume 52, Issue 7.
My elevation of Fox’s repudiation of the “eradication” meaning of herd immunity leans on Fine’s descriptions here and in his overviews of the herd immunity debates in 1993 and 1995. Even if Fine’s portrayal of the history of this debate is inaccurate, there is little question that he counts as a primary source on the matter, having assessed the subject while the debate was at its apparent height. And as Fine is critical of Fox’s 1971 paper in other respects, I felt reasonably confident in relying on his account.
Additionally, Fox’s model would go on to be essentially endorsed by Donald A. Henderson in 1987, suggesting that Fine’s account of the Fox paper having weathered the intervening decades is correct. More importantly, I hold that the 1971 definition of herd immunity, which repudiated the CDC chiefs’ absurd fantasy of eradication in favor of “the vague conference of some protection to a population,” is the only honest use of the term possible.
Further, other primary sources at the time seem to reflect Fox’s sentiment. One in particular is a paper by C E Gordon Smith, “Prospects for the Control of Infectious Disease,” presented at the Royal Society of Medicine’s 1970 Symposium on Problems of World Medicine. Smith provides a more intuitive approach to fatalism, than that constructed from Fox’s models a year later, categorizing diseases by categories of carrier and concluding that there are likely none for which the illusory “progress” of the era would get to a germ-free world (emphasis added):
The ease with which respiratory infections (e.g. influenza, common cold) spread even in highly developed communities suggests that measures designed to reduce effective contact are unlikely to be very successful, although reduction in overcrowding and better ventilation within buildings and other places where people congregate ought to help. As an example, however, the rapid spread of an organism so delicate as the meningococcus among America military recruits in modern barracks (Artenstein et al. 1967) offers little hope of controlling its spread in the great epidemic meningitis belt south of the Sahara by feasible improvements in housing. Thus vaccination seems to hold the most hope in the control of disease transmitted by the respiratory route […] However, if virtual absence of the disease is to be maintained, the proportion of susceptibles must then be kept below the critical level until there is no risk of reintroduction of the infection which, in these days of intensive travel, may well be until world eradication has been achieved - and this may be for ever in some cases. If therefor the requirement is to maintain immunity throughout life, and unless very long-acting vaccines are available, consideration must be given to the possible hazards of many repeated doses of a vaccine which although quite acceptable for use in a few doses, may not be suitable for many. […]
Complete eradication of all (and perhaps of any) infectious diseases in the foreseeable future is probably impracticable or too expensive either in money or resources, or in environmental devastation.
Smith goes on to offer a sober assessment of the risks of his era’s sudden, ongoing post-polio mania for a “vaccine for everything,” demonstrating that being a doctor does not mean that magical thinking about the potential hazards of novel medical interventions is actually mandatory:
Perkins (1969) has outlined the needs of safety testing: while reliable means exist for ascertaining whether a vaccine is safe in terms of acute complications, little is known about possible long-term hazards or indeed about how to test for them. This will undoubtedly require computerized records and ten or more years of careful follow up. The sooner the start is made, the better. With regard to virus vaccines there is no doubt that, in the short term, live-virus vaccines are effective and attractively cheap both in production and administration. But no live-virus vaccine is entirely safe and we are only beginning to suspect long-term complications from them. Highly purified vaccines containing only the necessary antigen(s) are becoming technically feasible but will be relatively very expensive. The constant recurrence of economic considerations in the control of transmissible diseases must not discourage us from research, however long-term, but these considerations should be kept in mind by all concerned.
Returning to the present: Professor Fine, for his part, has not been silent on the matter of “herd immunity” during the Pandemic Era, but neither has he appeared to seek out press attention. His attempts to clarify what his peers really mean by the phrase have been diplomatic. See McDermott, Amy. “Core Concept: Herd immunity is an important—and often misunderstood—public health phenomenon.” (2021, May 25.) pnas.org. Here Fine provides, as the most common-consensus expert meaning, the “disclaimer” version of the term - that it only means the moment when outbreaks (temporarily) reverse - and cautions that models cannot validly be used to calculate a value that will be true for everywhere at once, and should not presume perpetual surveillance for a virus with asymptomatic spread, without expressing the related fact that such models are what his peers keep using.
(I still have not gotten around to addressing the asymptomatic spread issue; suffice it to say I am aware that the JAMA paper asserting that it has been proven was horrid garbage.)
(index link anchor)
Interviewer question from “Smallpox Eradication: A WHO Success Story - Interview with Donald A. Henderson.” (1987.) World Health Forum, Vol. 8. p. 289. (who.int link.)
Topley, W. Wilson, G. (1922.) “The Spread of Bacterial Infection. The Problem of Herd-Immunity.” The Journal of Hygiene.
Topley and Wilson’s mistake of examining the effects of population-wide vaccination levels experimentally, rather than just asserting a bunch of model-sustained propaganda, is no longer repeated in our modern enlightened era. Additionally, their method of subjecting the mice to infection was so crude that the “experiment” was largely a failure.
Despite this, other modern sources appear to have misunderstood their results, presenting the experiment as some type of pioneering Mouse Manhattan Project that “discovered” herd immunity, launching a “mainstream” fad:
“By the 1920s, clever studies with hundreds of thousands of mice vaulted the idea into the mainstream, stirring optimism that making a fraction of a population immune could forestall a devastating outbreak.”
The portion of the Topley / Wilson study that included measurable outcomes - culture-confirmed “specific” mortality for the bacteria the mice were immunized against - for an actual model of “herd infection,” numbered 60 mice.
This is too bad. I had hoped to be able to incorporate the issue of “plagues” among livestock into my historical reconstruction of the herd immunity myth, in order to tease a parallel to the Immune Equilibrium model for plagues - that they are “caused” by the isolation, not crowding, of populations from each other (except for malaria; malaria is caused by mosquitos, objectively genocidal lunatics who think injecting microbes into other animals’ blood is a good idea).
However, it seems that modern veterinary medicine bears no influence on the adoption and development of the explicitly vaccine-centric Herd Immunity Myth at all.
Overall, the history of plagues among livestock has been more or less excised from the narrative Origin Story of modern medicine, but they were probably at least as important to the milieu of anxiety and desperation in which germ theory was born. An account provided by George Fleming in “Animal plagues : their history, nature and prevention,” for example, portrays everyday life in the 1800s as a ceaseless freak-show, a Boschian menagerie of medieval grotesqueries:
Sencer, D. et al. (1967.) “Epidemiologic basis for eradication of measles in 1967.”
“Susceptibles” is a now-outdated term for deplorables.
Oh… I guess that was pretty simple!
See Lahariya, C. (2014.) “A brief history of vaccines & vaccination in India.”
See Hinman, A. et al. (2004.) “Evolution of Measles Elimination Strategies in the United States.” The Journal of Infectious Diseases, Volume 189, Issue Supplement_1.
The authors ascribe a value for 1966 case-rates that seems unsupported by their own graphs; and seems to have been derived from nearest high-spike before 1966.
Fox, J. et al. (1971.) “Herd immunity: basic concept and relevance to public health immunization practices.” American Journal of Epidemiology.
https://www.behindthename.com/names/gender/feminine/usage/english/letter/i https://www.behindthename.com/names/gender/masculine/usage/english/letter/i
My characterization of Fox’s model is crude and simplistic; I have retained the heterogeneousness but discarded his structural, non-randomized framework, as it seems like overkill.
(Fine, P. et al. 1993, 1995, 2011.)
(Anderson, L.)
(Sencer, D. et al.)
The elevation of the obsession over “outbreaks” gives the lie. The field only centered its gaze on that goal so that it could play footsie with the true aim and claim innocence afterward. There was little to no outside pressure on epidemiology to make illness more “regular.”
A Google n-gram proxy for interest in outbreaks vs infection:
And as far as requests from outside for the field to provide advice for disease “control,” namely in the context of non-seasonal outbreaks of novel viruses, this in turn did not necessitate a fixation on “herd immunity” to a virus that is already widespread, since as per the consensus established after Fox, population-wide vaccination rates cannot play a role. Only a fantasy of eradication justifies resurrecting the debate.
But if my argument that epidemiology has been mired in self-deception is not convincing, the jury is encouraged to take the offered evidence and deliberate on the separate charge of intentional, malicious, one-way deception.
I could not possibly have written “collapsing” without unfolding into taunting and vulgarity.
(Hinman, A. et al.)
See footnote 15.
So now that China has approved an HIV pill to treat Covid, can we talk about the elephant in the room? https://www.reuters.com/world/china/china-allow-use-genuine-biotechs-hiv-drug-covid-patients-2022-07-25/
Early studies of the covid gene (and related patented genotypes) showed an HIV inclusion. It was chromosomal. But it was there. A bat virus never found in a bat in the wild, with an HIV componenet, now an HIV pill for covid.
You say:"I mean if you don’t think the 2013–2016 West Africa outbreak was the result of an undisclosed WHO-promoted experimental Ebola/Marburgvirus/HIV vaccine-induced antibody dependent enhancement debacle at this point, you’re probably crazy!"
Have you *any* evidence to back the idea that this is what happened?