Crackpot Corner: Marekspocalypse Edition

Widespread use of vaccines is courting a "Marek's Effect Spiral" of viral enhancement with no way back to normal - but not with coronavirus.

I have revised the wording of my thoughts on the distinction between immune-evading and non-immune-evading viruses in both “Die Herd” and my crackpot Immune Equilibrium essay, resulting in a formulation that I think is provisionally adequate:

1. 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).

2. 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.

I have as well, of course, already posted my argument for why this implies that Marek’s Effect will not occur with SARS-CoV-2 in “Forever Spike.” Readers more interested in the broad outline should read that essay first. The following is an expansion of those thoughts. However, this involves discussion of a theory that remains in a largely embryonic state, still predominately intuition-based.

I am nonetheless posting these thoughts for this reason: The prevailing situation is that most of the authors warning about a Marek’s disaster for SARS-CoV-2, and reading the tea-leaves of government statistics to divine whether it has already arrived, do not seem deeply curious about actual virology or the immune system - the factors which are actually at play when Marek’s Disease Virus gets inside a chicken, and either kills it or does not. Since this leads to flawed extrapolations, someone needs to wage the counter-argument. Otherwise - if the distributed effort to contort a coronavirus to fit the Marek’s Effect model continues - we’re soon all going to be running around with an even worse understanding of viruses than before (and that’s saying something).

The following text, therefor, will appeal to readers who aren’t sick to death of my Immune Equilibrium argument, and who regard my further development of the argument as non-obvious. Otherwise, feel free to move on with your day.

For those who continue: Again, the warning applies that this is the outline of research that is in-progress. Consider this intellectual freeware, to employ in your own thoughts and research as you would like. It is not an attempt to offer a locked and settled picture of reality.

Lastly, to be clear, I am not arguing for anything other than an immediate ban of these incredibly lethal pseudo-vaccines, and placing everyone who has promoted them in the town stocks for violating the Nuremberg Code, where most of them will presumably be physically attacked by angered parents for days on end.¹

What is at stake here, however, is whether the currently unvaccinated need to worry about losing out in an evolutionary arms race, because the “leaky” Covid-vaccinated are cooking up a “Super SARS-CoV-2.”

It isn’t going to happen.

When the doctor finally showed up (Oh boy!)
His fur was soaking wet.
He said that this should do the trick -
We hadn’t told him what the problem was yet.²

Onboarders

One day I will have a perfect metaphor for the immune evading distinction. For now, I am likely to regret the attempt. But here goes:

Let us think of the multicellular organism as a hotel. Viruses are genetic visitors, touring the countryside. They check in; they make a bit of a mess; they move on. The staff (the cells of the immune system) clean up afterward. If the guest makes too much of a mess, the staff put up a poster at the front desk. Eventually the same trouble-maker as before, wearing a mustache and a funny hat, sneaks past the desk; the mess is made again; the poster is updated.

Here we have described the incredibly simplistic model of the immune system that is used to sell the concept of vaccines in the first place: “Let Science show the staff this year’s version of the really messy guest in a tranquilized form - we’ll mark him with a funny scent that leads to a call to the manager. The front desk gets its mug shot, but you don’t have to worry about fixing any holes in the wall.” It’s an incredibly stupid idea - the immune system is not actually a hotel with a front desk! you cannot correctly train it with adjuvants instead of real cellular destruction! - but it’s made an industry, so what do I know. But setting the stupidity of using an oversimplified model to sell interventions into nature aside, the model functions adequately for describing routine, usually benign respiratory and gut viruses - the common cold, etc.

Fitting immune evaders into this model results in a total subversion. These are viruses which check into the hotel very shortly after the grand opening (i.e., in childhood), and, by the time they have had their face added to the front desk, have taken free residence in entire wings of the hotel, and have persuaded the staff of the hotel not to try to kick them out. These “wings” can be thought of as the virus’s biological niche - neurons, liver endothelial cells, or immune cells themselves, as common examples. Avoiding destruction of the niche depends not only on turning off replication - entering dormancy and integrating with host cells, or what is called “lysogeny” - but on repelling other viruses. Both these genetic talents can be likened to “upkeep” in the hotel model, even if lysogeny is only a passive form of upkeep. In my Immune Equilibrium essay, I applied the term “onboarded virus” to describe the viruses which successfully inhabit these niches; here I’ll simplify to onboarders.

Immune Equilibrium implies and predicts, firstly, that onboarders must devote most of their genome to their immune-evasion talents, and secondly that these talents must include sophisticated timers and sensors that allow the virus to calibrate the initiation and release of lysogeny to the immune system of the species it shares a “super-genome” with.³ These genes are what are distorted by vaccination. Here, “distorted” is still a very mechanistically vague notion, but I think I have already improved upon the hand-waving generally deployed when discussing how viruses become more allegedly “virulent” (and the even vaguer, semi-magical notion that they seek to become more contagious while being less virulent, because Darwin).

One fairly well-studied onboarder we can use as a model is betaherpesvirus 5, or cytomegalovirus. It is sometimes abbreviated “HCMV,” but as this is outdated I will use bH5, my own construction. Experiments in deleting large swaths of the bH5 genome reveal that only a portion of it is critical to the basic job of replicating within a cell. Deletion of some of the remaining, “nonessential” genes affects whether bH5 can acclimate to its normal, full range of cell types. But when bH5 is stripped of still other of these nonessential genes, it doesn’t become less competent at spreading through sample tissues - it spreads faster. From a 2003 study of the bH5 genome by Dunn, et al. (emphasis added):⁴

Our results showed that 45 [28%] ORFs [open reading frames] are essential for viral replication in fibroblasts and 117 [72%] are [partially or fully] nonessential. Some genes were found to be required for viral replication in retinal pigment epithelial cells and microvascular endothelial cells, but not in fibroblasts [connective tissue cells], indicating their role as tropism factors. Interestingly, several viral mutants grew 10- to 500-fold better[!] than the parental strain in different cell types, suggesting that the deleted ORFs encode replication temperance or repressing functions. Thus, HCMV encodes supportive and suppressive growth regulators for optimizing its replication in human fibroblasts, epithelial, and endothelial cells. Suppression of viral replication by virus-encoded temperance factors represents a novel mechanism for regulating the growth of an animal virus, and may contribute to HCMV's optimal infection of different tissues and successful proliferation among the human population.

Betaherpesvirus 5 can be an aggressive, destructive invader during fetal or neonatal infection, but is a benign guest if introduced during the rest of childhood or adulthood. In this, it resembles Rubella and HSV-1 and 2, other culprits of rare birth defects that are otherwise benign in healthy, well-nourished children and adults. Evaluation of blood samples from the 1988-94 National Health and Nutrition Examination Survey found that 36% of children aged 6 to 11 had antibodies for bH5; and 90% of individuals over 80.⁵ This does not mean that all of these individuals carry dormant virus - meaning that the virus has integrated itself with host tissue - but as bH5 could be the most sophisticated immune evader of all herpesviruses, universal onboarding after infection is possible. If betaherpesvirus 5 were a lethal super-bug, you would have heard of it before today.

But of course, the prevailing attitude in the research is that bH5 is responsible for all sorts of human ailments, despite being nearly universally encountered. It is believed, among other things, to “burden” the cellular immune system, and to “cause cancer,” similar to the liver-inhabiting Hepatitis B virus - a virus which inaccurately bears the condition of liver inflammation in its name even though plenty of people carry the virus in their liver cells with no issue. (Humans, if they were to apply to themselves the same standard applied to viruses, would presumably have to be renamed “Submarine Crash B organism.”) The question of whether onboarders do in fact instigate chronic disease, or whether there are geographic co-evolution factors between onboarders, the microbiome, and the human diet that the modern, globalized world throws into disarray, can be set aside for now.

What is relevant for this discussion is that the genome of bH5 dedicates a large share of programming to the preservation of “temperance” in the context of its niche - the tissue and species which its particular set of proteins and replication pathways allows it to inhabit. Neither of those things - tissue and species - are separable from their corresponding immune system. Viral immune evasion and temperance genes are merely the constituent elements of an overall logical architecture - a sophisticated, adaptive pattern-recognition algorithm which is likely older than multicellular life itself.⁶ This architecture, after all, is already apparent in the genomes of the viruses that coexist with bacteria (phages), which successfully alternate between replication (and host cell destruction) and lysogenic integration with the host cell, in response to quorum-sensing peptides and other signals indicating the condition of the colony - some of which signals can only speak in patterns, not in semantic symbols.⁷

The immune suite of a bacterial cell is not the same as the immune system of the human, which is not the same as the immune system of a chicken. And the immune system of a vaccinated chicken is not the same as the immune system of an unvaccinated chicken.

Turning back to Marek’s Disease (Herpes-) Virus, a single infection is possibly enough to prompt the rewriting of the MD(H)V evasion and temperance timers. Or, it may take a few generations of serial passage - with only the “up-tuned” strains of the virus successfully transmitting to other vaccinated chickens - before there is a meaningful change. Either way, the default temperance of the virus has been altered in some manner. It may be as simple as lowering suppression of replication, so that the virus can “outpace” the vaccinated immune response, or it may be something more complicated. The result - an immune evading virus which is no longer acclimated to its niche species as born, leading to high fatality among unvaccinated chickens - speaks for itself, so it is not necessary to nail down the specifics.⁸

This has profound implications for humans. Gobs of the viruses currently being targeted for future “vaccine” rollouts are herpes and hepatitis viruses. And several current vaccines target immune-evading viruses, and are possibly or probably already leading to the development of future super-viruses.

This includes the vaccines for measles⁹, mumps¹⁰, chickenpox (a herpesvirus), and Hepatitis B Virus.¹¹ Any or all of these could lead to a future where unvaccinated children are vulnerable to a lethal, “overclocked” version of the virus, and where, possibly, even vaccinated children in some regions of the world will not be safe from visitors from “hotter” regions. All of these were already treatable during cases of severe (childhood) infection before their corresponding vaccines were promoted by moronic, incompetent health authorities.¹² Vaccination against these and all other viruses, as a general practice, should be halted everywhere in the world immediately, and thrown into the dustbin of retired medical nonsense with lobotomies and mercury cures.

The last general comment to make about onboarded viruses, before moving on, is that they reactivate. To return to the hotel metaphor, if the onboarders in their conquered wing start to notice that the walls are cracking, or perhaps that the original “staff” of the immune system is suddenly rushing off somewhere as if to reply to a fire, it is plausible that they “interpret” this (are genetically programmed to act as if doing so) as a signal that the hotel is near the end of its service.

Here the model virus par excellence is chickenpox, or “varicella-zoster virus” - again, a herpes virus. Here we will use the newer, but still conventional designation HHV-3; as all that I am concerned with is keeping the “H” visible. During original infection, HHV-3 enters dormancy upon spreading from the primary site of infection into human nerve cells. Here, we must praise the discernment of the virus’s “superfluous” genes - almost any amount of replication in nerve cells would likely lead to inflammation and consequent myelitis and paralysis, yet childhood infection with HHV-3 is largely a trivial event.¹³

When perceiving signals of tissue distress later in life - such as induced by an injected mRNA script for a spike protein that leads to widespread cellular disruption and destruction - HHV-3 leaves dormancy and transits from nerve cells to epithelium. Here it begins to replicate again, leading to the outbreak of rashes on the skin known as shingles. These go on to self-transform into dried particles that can shed the virus to other humans, similar to MD(H)V in chickens. The virus, in other words, stops worrying about preserving the survival of the hotel / host, and makes a bid for getting out.

This bid may be halted midway, if the immune “staff” return to prompt the virus to resort back to dormancy. Either way the result is the multiplication of possible transmission events in the lifetime a single host. We need not assert that dormancy is an entirely “altruistic” talent on the part of the onboarder genome.

The signs all flicker and buzz all night
Passing by you could hear them say, “Hey!
Please won't you just come on in?
Won't you please just go away?"¹⁴

One Night Stand

Coronaviruses, unlike herpesviruses, do not seem to possess (cellular) immune evading traits (or these traits are effectively suppressed by onboarded viruses which have already “staked a claim” in the host¹⁵).

Moreover, as mentioned in the Immune Equilibrium argument, there is not any strong reason why coronaviruses would try to evade the (cellular) immune system. To repeat the portion of the argument not already excerpted:

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.

In this argument, not only do coronaviruses match and play by the rules of the “simplistic” hotel model - they evade the front desk by a gradual change in appearance - they occasionally arrive to the same hotel to find the front desk (mucosal IgA antibodies¹⁶) empty. While the “staff” - the T Cells roaming the halls, the quickly alerted B Cells which stimulate ramped up antibodies, etc - are sufficiently familiar with the virus to prevent a severe course of infection, there is at least enough of a “mess” to prompt an update to the photo at the front desk, and redouble shifts (antibodies) for a few months while the hall staff rests up.

So far, there has been evidence of SARS-CoV-2 taking residence in at least some immune cells.¹⁷ This does not appear instrumental to the SARS-CoV-2 phenotype. The broad, innate immunity of children, which is based in part on effective suppression by Natural Killer Cells in the respiratory epithelium, robustly demonstrates that SARS-CoV-2 does not (like Measles and other childhood viruses) make immune macrophages its niche. Nonetheless, it may still possess certain codes for immune evasion somewhere in its long genetic program.

But this provisionally does not matter, since the argument above posits, critically, that host (human) adaptive cellular immunity does not meaningfully engage with the coronavirus genome.

To return to the “ideal” bH5 model of onboarders, the genome may be divided crudely into 4 parts (graphics to be added later):

1. Genes for producing future viral elements (polymerase, proteins, etc).

2. Genes for intracellular immune suppression.

3. Genes for cellular immune suppression.

4. Genes for temperance.

Category 1 is sensitive to antibodies, especially mucosal IgA. Category 2 is not related to the adaptive immune system at all (the firewalls inside your cells that guard against viral replication do not rewrite themselves after a prior infection; the genetic machinery viruses use to circumvent those firewalls are thus not subject to evolutionary pressure, but instead are basic elements of viral competence).

Categories 3 and 4 are sensitive to host cellular immunity, and are thus subject to pressure by vaccinated hosts, leading to “overclocking.”

This can be compared with the SARS-CoV-2 genome:

1. Genes for producing future viral elements (polymerase, proteins, etc)

2. Genes for intracellular immune suppression.

3. (Possible, inert) genes for cellular immune suppression.

With no need for temperance genes, Category 1 is probably always tuned to functionally maximum levels. In other words, SARS-CoV-2 is already already trying to multiply as quickly as possible in order to favor maximum infectivity and transmission. It can afford to do so without any danger of killing off the host, because it is functionally vulnerable to (innate and adaptive) cellular immunity. Further, Category 1 is the most effective realm for innovation in response to adaptive immune pressure. If the virus is confronted with “neutralizing” IgA antibodies, infection and transmission will favor novel changes to the spike protein. (This is the basis for stating that adaptive cellular immunity does not place pressure on the coronavirus genome.)

Category 2 is exactly as insensitive to adaptive immune response in SARS-CoV-2 as with an onboarder.

Category 3 is where our interest lies. Would encounter with a Covid vaccinated immune system, somehow, exert pressure on this element of the coronavirus genome?

The answer does not require resort to theory. It has already been demonstrated by the experience of our reckless mass experiment. To the extent that the Covid vaccines, in the first few months, exert pressure on the virus, it is in the direction of spike innovation. After the first four or so months, in regions without “boosting,” this pressure has likely ceased entirely. The Covid vaccinated are just as capable of infection and transmission as anyone else - in fact seemingly more-so.¹⁸

Moreover - in fact, almost brilliantly - the adaptive cellular immunity response induced by the Covid vaccines actually places less pressure on the SARS-CoV-2 genome than does natural (post-infection) immunity!

By only training the immune system against the spike protein (or, in the case of the vector vaccines, a combination of the spike protein with nonsense adenovirus proteins), the Covid vaccines ensure that adaptive cellular immunity is less, not more competent than it would be after natural infection. Natural infection prompts the development of a kaleidoscopic spectrum of T Cell phenotypes, which migrate to the tissues of the respiratory and digestive tracts to monitor for every one of the proteins which, if displayed on the surface a cell infiltrated by the virus later, would trigger the T-cell to destroy the cell and stop infection. Not only are these T Cell responses more wide-spectrum than the spike protein alone; they select more for the basic, essential proteins of coronavirus which cannot be modified without loss of function.¹⁹

In natural (post-infection) immunity, the pressure exerted by adaptive cellular immunity (Killer T Cells) is flexible, creating a permissive environment where the virus can survive without being forced to take on (cellular) immune-evading traits. In Covid-vaccinated “immunity,” that pressure doesn’t exist at all! The Covid vaccinated are placing less (cellular) immune escape pressure on the SARS-CoV-2 genome, therefor, than the unvaccinated. They in no way can prompt the reactivation of inert immune escape genes.

The virus could spend a thousand years passing between the Covid-vaccinated, therefor, and those of us still carrying around the immune system with which we were born into this world would have nothing to worry about.

Or, at the least, the onus is on those who would argue that Marek’s Effect could apply to SARS-CoV-2 to actually model how the genome could be modified by serial passage through Covid vaccinated individuals. Otherwise, all these vague references to some universal element of viral “contagiousness” that is distinct from “lethality” do not constitute a true mechanistic explanation for why such a thing should occur.

In the meantime, oranges are being used to sell readers an apple.

Immune evading viruses place themselves in an existential quandary, which must be solved by the development of sophisticated genetic algorithms for temperance. With onboarders, it is the virus that preserves the survival of the host.

For non-immune evading viruses - which may in fact be former immune-evaders who were “domesticated” by the refinement of animal antibody structures - there is no such need for genes devoted to temperance.²⁰ Here, it is the host genome which preserves the survival of the virus; and by doing so, renders the viral genome essentially “blind” to adaptive cellular immunity.

And as if that was not enough, “vaccination” against the spike protein alone is essentially the same as the disablement of cellular adaptive immunity. It removes even the possibility of pressuring the virus to escape the protective immunity of the innate and adaptive cellular immune system.

1. Not jail. In Defense of Flogging.

2. Brock, Isaac. “Shit in Your Cut.” Strangers to Ourselves. Epic, 2015.

3. To quote from “Burned All My Notebooks,” my Immune Equilibrium essay:

Super-genome: An overall genome as comprised of both endogenous and viral shares of genes.

4. Dunn, W. et al. (2003.) “Functional profiling of a human cytomegalovirus genome.” Proceedings of the National Academy of Sciences USA. 2003 Nov 25; 100(24): 14223–14228.

5. See Staras, S. et al. (2006.) “Seroprevalence of Cytomegalovirus Infection in the United States, 1988–1994.” Clinical Infectious Diseases, Volume 43, Issue 9, 1 November 2006, Pages 1143–1151.

6. And, again as suggested in “Burned All My Notebooks,” plausibly instrumental in multicellular embryogenesis.

7. Which contributes further to the suggestion, in “Burned All My Notebooks,” that onboarded viruses are a plausible source of genetic stability - a reservoir for genes that need to be insulated from natural selection to ensure longterm survival of the super-genome, including psychological and social genes.

8. If I were prone to label-izing everything, I could propose that Marek’s Effect be replaced with the term Vaccine-Induced Super-Genomic Crash.

9. Measles does not appear to have any “superfluous” genes. It appears, therefor, to be in a separate category of immune evader that may not actually “onboard.” Or, there may be discrete (circular) genes that have not been discovered; or it may interact with human genes that supplant the measles virus phenotype with onboarding traits (such as the gene for viperin; see footnote 10). I am skeptical of the extent of our knowledge of measles; it is necessarily challenging to research how the virus behaves in a natural state since the vaccine is over 50 years old, and likely that interest in such research is not great. The association between measles vaccination and the instant rise to preeminence of rubella - prompting, what else, the promotion of more vaccines - suggests measles is capable of some type of niche inhabitation, similar to onboarding - despite very little apparent overlap in the two viruses’ pathways (beyond being respiratory viruses that affect children).

As stated, this is all still a theory in development.

10. Mumps, more than measles, is plausibly an onboarder, and more than chickenpox (HHV-3) plausibly already out in the world as a vaccine-enhanced super-virus. Measles and mumps are collectively where I currently have my money for the viruses whose vaccination creates susceptibility to the “modern plagues” of HIV, Ebola, etc. - viruses which are more plausibly ancient and benign than novel and immune-disabling.

Here, again bH5 is a model of how such a phenomenon could operate (though there is not yet a vaccine for bH5, despite efforts to the contrary), even without reference to the herpesvirus’s extensive set of “temperance” genes.

The bH5 glycoprotein (analogous to the spike protein), once produced in invaded immune cells, stimulates the cell to produce the Viperin protein - Viperin not only inhibits further production of bH5, but numerous other modern monsters-of-the-week including West Nile Virus, HIV, and Influenza. Viperin-stimulation, therefor, can be thought of as a means for immune-evading viruses to stake out their niche (in this case, immune cells themselves) and lock out later invaders during adulthood.

This, once again, merely refers to a genetic talent that has already been observed in bacterial viruses (phages), and is thus a part of the viral toolset that is older than multicellular life and the immune system itself. So it is more outlandish not to imagine that childhood infection with measles and mumps, etc. protect us from adult-onset immunodeficiency, and that vaccination disables this protection, than the reverse.

11. Hepatitis B and C viruses are superstitiously believed to “cause” liver and other cancers based, it would seem, entirely on a handful of studies from the 70s and 80s that have never been questioned in spite of the modern Replication Crisis. There is no way to prove or disprove that infection leading to genomic integration (lysogeny) with HBV and HCV are not widespread in individuals that do not go on to have cancer, so it is just assumed as false (sampling of blood donations for antibodies may be based on the higher thresholds associated with reactivation of the virus, and further does not tell us the scale of infections that lead to dormancy). Additionally, even if it is true that infection and lysogeny with HBV is carcinogenic, that implies nothing about whether vaccination results in an improvement in clinical outcomes for cancer.

But the twin assumptions of infectious etiology and benefit of prevention, absent any attempt at verification, were nonetheless responsible for the literally worldwide, overnight promotion of a vaccine for a virus that almost no one even knew they had. There still does not appear to have been a single study demonstrating a reduction in cancer for the HBV “vaccine” in its three decades of use, despite widespread assertions of its efficacy.

In an overview of Hepatitis and liver disease in India, higher rates of vaccination over time merely result in a reduction of the association of liver disease with Hepatitis B. See Guatum, R. “Current Scenario of Hepatitis B and Its Treatment in India.” Journal of Clinical and Translational Hepatology. 2017 Sep 28; 5(3): 277–296. However, as observed rates of liver disease in India have increased by something like ~10 fold since the rollout of the HBV vaccine two decades ago due to the twin factors of increased observation and increased “lifestyle diseases” in general, this signal can be called ambiguous at best (clinically confirmed cases for “jaundice” reported to the federal Ministry of Health were a mere 110,000 in 1994 (who.int pdf, page 5) deaths for liver cirrhosis were ~400,000 in 2014 using the death rate (who.int) and India’s overall population).

Meanwhile, a recent trial for a Hepatitis C vector “vaccine” observed no difference in outcomes. Outcomes in the trial and control group were exactly equal (and of course, any difference in long-term cancer outcomes could not possibly have been measured to begin with). See Page, K. et al. “Randomized Trial of a Vaccine Regimen to Prevent Chronic HCV Infection.” New England Journal of Medicine. 2021 Feb 11; 384(6): 541–549.

In fact, since 1980, rates of liver cancer seem to have increased everywhere the HBV vaccine has been promoted except parts of east Asia. (McGlynn, K. et al. “Global epidemiology of hepatocellular carcinoma: an emphasis on demographic and regional variability.” Clinical Liver Disease. 2015 May; 19(2): 223–238.) Additionally, the HBV vaccines do appear to already be driving escape mutants on a global scale (Qin, Y. Liao, P. “Hepatitis B virus vaccine breakthrough infection: surveillance of S gene mutants of HBV.” Though, my reading on this subject is quite superficial.

The Hepatitis B vaccines are hot garbage; they do not work, and they may be leading the world to a future disaster where different populations cannot even safely be around each other based on disparities in their local viral “hotness.” They need to be banned.

This tangent, of course, deserves its own post. At some point I am likely to delve into non- Covid vaccines in more detail, but much has obviously already been written elsewhere. (Additionally, Colleen Huber has begun the same project, starting with smallpox.)

12. To quote, again, from the actual CDC presentation used to launch the first failed Measles Eradication campaign in 1967:

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.

13. And could, in fact, be a key element of psychosocial development, as alluded to in “Burned All My Notebooks.” I am still of two minds whether my hypothetical “Collaborative (as in viral) Psychosocial Genome” is more likely to be directly or indirectly (maternally) expressed. At all events, the former would implicate the chickenpox vaccine (the more widely-used version of which was rolled out in 1995) in you-know-what.

14. (Brock, Isaac.)

15. See footnote 10.

16. For a discussion of the importance of mucosal immunity in the distinction between competent natural memory immunity and semi-nonfunctional “Covid vaccine immunity,” see Boostermania. But even though reinfection after natural infection is so rare, and often subclinical, than on an individual level one might as well disregard it, the proof for the relationship between waning natural immunity, occasional clinically measurable reinfection (symptoms and transmission) and promotion of long-term viral survival, is in seasonal waves (of which I still need to write more, in my belated follow-up to “Burned All My Notebooks”).

17. This may be related to “Long Covid,” but I am skeptical.

18. See, again, “Forever Spike.”

19. Which is the entire reason antibodies must fade enough to allow later infection and transmission, in the Immune Equilibrium argument, to disincentivize (cellular) immune escape. Resident T Cells and Natural Killer Cells (“resident” refers to the cells which have migrated to the respiratory and gut epithelium to act as sentinels against infection), meanwhile (as mentioned previously), are on their own excellent at suppressing small flare-ups, but can still be overwhelmed by a large viral dose, as would normally only be encountered during seasonal surges.

20. This, provisionally, applies to poliovirus - my prediction is that the polio vaccine does nothing to reduce lifetime occasional (subclinical) reinfection and transmission. Thus, despite decades of use, the poliovirus does not appear to be subject to a Marek’s Effect.

The overall goal of my research is to define which features both determine and define when a virus does not need immune-evading traits to ensure survival, and see if this can be used to determine a point in the evolution of the multicellular immune system where promotion of viral survival becomes a “talent” of the endogenous genome. For now, I would bet that the general traits that such viruses likely share are use of the high-transmission respiratory and gut infection pathways, and predominate use of receptor-mediated endocytosis for cellular entry (not that these are limited to non-immune-evading viruses, just that they are necessary to ensure the survival of viruses that cannot evade cellular immunity).