From the co-author of the first peer-reviewed paper examining a laboratory origin for SARS-CoV-2, as well as its addendum, which formally linked the H1N1 Spanish Flu pandemic strain release of 1977 to gain-of-function research.
LabRoots.com
Part II - “You’re not actually mammals.”
Nothing marked the emergence of SARS-CoV-2 more than paradox: A near-certain zoonotic emergence in a Wuhan wet-market in December turned into an origin uncertain both temporally and geographically, a zodiac of possible intermediate hosts shifted from snake to pangolin back to bat and then on to mink and badger. And there was a debate for roughly a year as to whether the most obviously transmissible virus in human history was in fact airborne, after it first took priceless weeks to even declare that sustained human-to-human transmission had occurred at all despite the fact that the virus has already infected every industrialized nation on earth by early January 2020, and possibly earlier.
In addition to behaving like “no microbe humanity had ever seen” according to the doctors treating its infections, SARS-CoV-2 also elicits sequalae in novel constellations which often seem almost like they’re produced by combinations of different classes of virus – affecting the lungs, heart, kidneys, brain, and even the testicles.
Although its genome may lack any direct evidence of molecular engineering, if SARS-CoV-2 does leave fingerprints, they are of unexpectedness, novelty, and paradox. For instance, it is the first human coronavirus with a “flat and non‐sunken surface of its sialic acid‐binding domain… [and lacks] non‐synonymous substitutions in its RBD, which would be expected to accumulate at some point during a virus's natural evolution due to challenges from a novel host's complete immune system, but which would not be selected for and then observed to occur at the same frequency during cellular serial passage or during the few generations of whole host passaging required to establish airborne transmission.”[i]
So although SARS-CoV-2 doesn’t have the distinctive molecular fingerprints of intentional engineering, there are an awful lot of very suspicious smudges. But it’s far from the only virus which displays paradoxical behavior, as the inexplicable disappearance of the seasonal flu across much of the planet should have reminded humanity that we still do not know the source nor the exact sequence of the deadliest influenza ever to visit us: the pathogen behind the 1918 Spanish Flu Pandemic. However once again the duality of quasispecies swarms once again provides possible answers to all of those mysteries.
6.1 – “There is no swarm”
Social distancing and other public health measures like mask mandates have been implemented in a haphazard mosaic of political influence and scientific guesswork across much of the planet, however despite the appearance of any sort of unified actions against it specifically, that the seasonal flu all-but disappeared in many nations on earth, those hit by the pandemic hard and those barely touched by it alike.
However this can be explained by considering the roughly ten thousand years of agriculture once-avian influenza viruses have had to adapt to their human hosts, resulting in their mutation into endemic strains acclimated to humans which are not known to jump back from us into birds. These endemic strains have formed quasispecies mutant swarms which seek a sort of allostasis among their human host populations, remaining virulent enough to spread into enough new hosts to remain viable, with this virulence being enough only to kill primarily the aged and infirm.
Having reached an equilibrium with their hosts, quasispecies swarms of human influenza strains evolved to live alongside the relatively constant level of social interaction undertaken by their hosts, evolving in and around us as our societies got more complex and denser. The seasonal flu never actually goes away, it just goes into hiding when there aren’t enough transmission events due to environmental conditions - demonstrated by this recent study that concluded nearly half of all symptomatic influenza infections are caused by asymptomatic transmission, meaning the virus has no trouble at all spreading from people who don’t even know they’re infected. And by the middle of 2020, although the world was completely interconnected it hardly shared much in terms of public health policy.
But all the same, anyone living in the modern world would be at least aware of the ongoing pandemic and modifying their behavior to some extent. And although plenty of individuals decided to carry on as usual, most communities on earth witnessed some reduction in the average level of social transmission as public buildings and spaces closed and masks were worn. Not necessarily by everyone, but by enough of a change to create too much distance between human influenza quasispecies swarms to form in the drier, and hence more virally hospitable, winter indoor spaces as usual – when their infections begin to noticeably climb once the temperature drops.
This pattern would not appear if the current paradigm of individual strains holding static genomes that spread RNA viruses each and every instance there was the proper level of exposure was true. Although multiplicity of infection (MOI) has classically been used to measure the odds that a viral exposure would lead to infection, this measure would be far more accurately attuned if it was tuned to take into account the epistatic effects that emerge from quasispecies mutant swarms, since the total amount of exposure will often be much less important than the ratio of different variants that a host is initially exposed to. The other side of this phenomenon also explains why the SARS-CoV-2 pandemic has been accelerated not by super-spreading individuals, but by super-spreading situations.
This is because the diffused quantum nature of the statistical clouds formed by quasispecies mutant swarms means that the underlying epigenetic relationship between different variants becomes intensified when multiple hosts are transmitting their variants among each other simultaneously.
In this way, super-spreading events are larger fractal kaleidoscopic expansions of what happens within immunocompromised influenza patients – quasispecies-based infections increase in pathogenicity as more and more adaptive variants, which by definition start off as minority strains in whichever swarm they are found, are able to interact with the greatest number of other rare variants, some of which by definition will be adaptive and create epistatic interactions.
In the case of immunocompromised patients, once their organs are unable to restrict the swarm its hosting to predominately produce the strain best suited to it, mutant strains are able to migrate to other organ systems, where they mix and match with other sometimes adaptive variants – and so densely packed public spaces with poor ventilation become massive anthropomorphized immunocompromised COVID-19 patients, since while a single household may only measurably spread one variant, when members of myriad households gather together, the odds of more adaptive variants coalescing in the same swarms increases exponentially.
And due to the amplification that occurs as more and more hosts are added for a quasispecies swarm to spread into, packing unnatural concentrations of hosts together can lead to phenomenon like the emergence of highly pathogenic avian influenzas (HPAIs), which are only known to emerge from poultry farms, where high population concentrations mean that variants spread easily between new hosts effectively creating one shared quasispecies cloud of variants, and perhaps even more tellingly: Sick chickens are unable to self-segregate on commercial farms.
The immunological dynamics of unnatural population densities and the inability to isolate is mirrored very closely in many modern human industrial environments, which is a large part of why until World War II most of the deaths experienced by military combat units were due to infectious diseases and not actual combat, where 80% of the deaths following combat were from gangrene and not the wounds themselves.[ii]
And as anyone who’s been a medical janitor in an industrialized institutional setting such as the military or large and particularly girthy penal facility can tell you, these scenarios inevitably breed disease whenever there’s overcrowding on these wards – tempers flare and first a food tray and then a wheelchair fly across the room while an inmate with one functioning arm chases another inmate hopping around on one leg with his own walker and the poor medical janitor is huddled in the corner desperately trying to protect his tray because its taco night and watching in dismay as another food try goes flying across the top of a wall because that one was full when it started its flight and that’s definitely going to suck to clean and would’ve been delicious.
So in industrialized settings of all kinds, the specter of disease looms much larger than it does out in public. But as any doctor can tell you, if there’s a way to make a buck off of something, the medical community will do whatever as can to print as many dollar bills as it can, while convincing itself that its truly in the name of altruism. Or at least a minority will, while the rest stand by and watch.
Y’all got any more of them opioids?
6.2 “First, do no harm.”
So for no reason other than to try and create a drug which is could then bring to market and sell, a company named Medimmune took a live-attenuated influenza vaccine strain originally designed with NIH funding, which there was no immunological need for whatsoever since the extant inactivated vaccine had been incredibly effective for decades, and created a nasal-spray drug called FluMist in 2004, which it seemed to want to market to kids since they might be afraid of needles and “need” a nasal spray vaccine.
Medimmune would be sold to AstraZeneca in 2007 for more than $15 billion dollars and other perks like box-seat season tickets to the Redskins and Orioles for its executives, primarily for access to FluMist’s patent, since its sales regularly brought in tens of millions of dollars in raw profits. Great news for the executives and stockholders involved, especially since FluMist brought in over $100 million in sales for AstraZeneca the year after its purchase, but terrible news for the kids actually given FluMist, many of whom weren’t protected at all.
Since it turns out, that once again an experimental and epidemiologically unnecessary vaccine would go on to harm many of those first exposed to it – leading to infections where none would’ve occurred with the regular, cheap, old, inactivated vaccine injected by a needle as it had been for generations. And the CDC and the American Academy of Pediatrics will likely continue to go around in circles about FluMist’s efficacy[iii] as various lobbying groups compete against each other, despite the fact that AstraZeneca has been directly asked to explain the fact that FluMist often seems to confer no protection, and come up with “because money.”[iv]
Because the communal and social changes required to blunt quasispecies mutant swarms aren’t something anyone can guarantee they’ll make money from, and so scientific research into them has been extremely limited. And of course an airborne respiratory virus is a terrible candidate for a live-attenuated vaccine due to the quasispecies swarming dynamics which allow rare variants to quickly reinforce extant ones, and never would’ve been attempted at all if not for the monetary temptation and willful blindspot around quasispecies mutant swarms pushed by pharmaceutical companies directing research dollars away from it.
Sure in theory it makes sense and FluMist might work in small trials, but the social nature of quasispecies swarms means limited lab results simply can’t be extrapolated to society as a whole if you’re ignoring the quasispecies swarming effects. However the development, sales, and ultimate failure of FluMist reinforced an important concept in the modern age of genetic engineering – there was always money to be made designing vaccines which aren’t necessarily needed and will effectively harm people because they don’t provide protection or even worse may deattenuated into vaccine-derived-viruses, so long as they can be marketed effectively.
Find the right scientists to design and market a vaccine, and depending on the nature of the disease that it’s supposedly protecting against, you may just have created yourself a bottomless ATM. And everyone who profited off FluMist set the stage for our current pandemic, demonstrating to pharmaceutical companies across the rest of the planet just how much money could be made from pushing a vaccine that there wasn’t even the vaguest shred of demonstrated need for – especially if it was a live-attenuated vaccine, since they offer the best possible protection when done correctly, and could be marketed to replace inactivated ones just like FluMist was.
6.3 – “Bubble, bubble, toil and trouble...”
And those pharmaceutical companies designing vaccines proved without a doubt during the COVID-19 Pandemic that their primary interest is making money, not preserving human life. And it’s not that there’s necessarily anything particularly dangerous about the new class of mRNA vaccine, it’s that to allow the emergency use authorizations which allowed their quick development and distribution – no other sort of therapeutic could be designated as effective against the novel coronavirus.
So the fact that many Americans, and especially our poorest and most vulnerable minority communities, have vitamin D deficiencies which predispose them to all sorts of diseases,[v] and just about everyone who eats an industrial diet runs a selenium deficiency which profoundly weakens their immune systems – none of these basic nutritional realities were addressed by America’s public health authorities in the slightest.
It was all vaccines, all the time.
Whether or not double-blind studies have demonstrated vitamin D and selenium’s efficacy against COVID-19 in particular, the obvious biological pathways they harness and their proven efficacy against other viruses would’ve made them an immediate go-to by a government not having its strings pulled by pharmaceutical companies who seem pandemics as multi-billion dollar epidemiological carrots.
Both selenium and vitamin D are very safe and dirt-cheap to manufacture and sell, not to mention other extraordinarily safe supplements like zinc which bolster immune function, but if offered altogether and distributed as an effective prophylactic treatment they would’ve sidelined the “emergency use” nature of vaccine development that expedited or eliminated the usual testing and other requirements.
Instead of simply and cheap public health measures, our government went with confused messaging around masks, and an all-out press to convey vaccines as the Holy Grail of immunological protection, when what was being designed was a brand-new form of untested mRNA pseudo-vaccine which only targets one of SARS-CoV-2’s surface proteins and not its entire genome – a strategy that is destined to fail at the community level unless massive public health changes are made, based on everything modern science has learned battling highly transmissible RNA viruses like the avian flu and IBV on poultry farms.
An effective vaccination program requires surveillance, introducing a vaccine which only targets part of a virus’s genome when that virus is already spitting off escape variants isn’t a strategy to save lives, it’s a strategy to buy a little time while monetizing the never-ending need for booster shots and ensure that mostly the poor and disenfranchised slowly die off as they’re crowded into closer and closer living and working conditions.
Meanwhile, basically by accident, and without anyone even trying at all and clearly not due to vaccines or any other pharmaceutical product that was sold to anyone, seasonal influenza pretty much disappeared across the entire world. And while pharmaceutical companies made billions in profits from a novel untested vaccine technology with no demonstrated long-term community-wide efficacy, and began to count billions more emerging along with new variants, American souls have slowly been extinguished in their beds in their quiet hundreds of thousands.
In between counting their billions, these vaccine companies seemed to have forgotten to tell the rest of us that when they try to vaccinate massive poultry farms against influenza, an airborne RNA virus that is so much less transmissible than COVID-19 that it nearly disappeared from humanity entirely when we communally adjusted our public health habits just slightly in response to the pandemic – it is still functionally impossible. Even with full surveillance and bespoke vaccines, highly virulent strains that kill half the population of birds still emerge on large-scale commercial poultry farms since transmission is inevitable, and transmission means the quasispecies swarm is given a chance to adapt and grow hotter.
So if influenza can’t be eradicated from poultry farms even when highly-tailored inactived vaccines designed against the full genome of avian flu, and not just one protein like COVID-19’s experimental mRNA vaccine targets, administered alongside comprehensive surveillance programs that allow for the sickest hosts to be isolated in a cage – how is this pandemic almost over?
Why is this new unproven mRNA vaccine technology going to eradicate COVID-19 when millions of transmission events are still occurring each and every day all across the globe, so besides its accelerating mutational profile: How is a vaccine that only targets part of its genome going to eradicate this pandemic, when even vaccines that are administered without any consent at all on chicken farms which target entire genomes can’t eradicate airborne RNA viruses from them?
Unfortunately for poor people, the pharmaceutical companies don’t care how many of us die so long as they’re raking in their endless billions, and even though COVID-19 managed to take out the luxury mink farm industry in almost a matter of weeks, that luxury market is so much comparatively smaller than Big Pharma that no one really questioned how a pathogen had just managed to start the first interspecies pandemic the world had ever seen, in a species that isn’t particular close to humans at all.
7. “With each crime and every kindness, we shape our future.”
1776 marked the birth not only of a political document, but it was also the year that Dr. John Morgan, Physician-In-Chief of the fledgling American army wrote the first Treatise on Variolation, part of General George Washington’s successful variolation of his troops against smallpox. This vaccination effort began what was almost certainly the world’s longest continual vaccination program against a single disease, as it persisted for over 200 years into the early 1990s, 20 years after smallpox had already been considered eradicated in the civilian population.[i]
Luckily for humanity, smallpox only came in a single serotype, or broad category based on a host’s immunological response to it. Serotypes are immunological species at least in the sense that our immune systems never have to worry about responding to any version of smallpox other than the one that’s always existed, its swarm is potent but not particularly diverse.
On the other end of the quasispecies spectrum is an RNA virus like Dengue Fever (DENV), which is arguably the viral world’s malaria, since like the parasite the causes malaria it needs to be vectored by an arthropod – both dengue and malaria use mosquitos, others use ticks – and it’s had an extensive history interacting with and affecting human societies. DENV comes in four very distinct serotypes, functionally four distinct quasispecies swarms as far as our immune systems are concerned.
And since as an arbovirus DENV must be passed into us by a vector its quasispecies swarm adapted to this intermittent pattern of exposure to prospective new hosts by developing these four serotypes. And it turns out that although the first infection will appear to have a diverse and heterogenous example of any one of the four serotypes’ swarms, curiously the second more symptomatic and lethal infection seems to appear after a fresh DENV quasispecies swarm infects someone a second time – leading to a selective process where more antibodies enhance the quasispecies swarming infection rather than neutralize it, and a more homologous and acutely infective quasispecies cloud that mostly represents one of the four serotypes instead of being a more balanced mix of the four like initial infections seem to be.[ii]
Get infected by a quasispecies swarm primarily representing one serotype and you’re protected from its entire subfamily for a good long while, but get protected from the other three serotypes only temporarily. And once this temporary protection wanes, a second infection of DENV by a quasispecies swarm primarily representing a different serotype often leads to antibody-dependent enhancement (ADE), a phenomenon which seems to account for Dengue Fever becoming lethal as its thought to be behind about 90% of all symptomatic cases.[iii]
And probably starting with Alexander the Great, as the world’s militaries eventually figured out after millennia of attempting to invade mosquito-infected regions – it’s impossible to create a vaccine or any other ingestible prevention against Dengue Fever – the only attempt to make one using the related Yellow Fever one as a template resulted in a strain that quickly deattenuated back to its virulent and fully neuropathic V-1ooo form.[iv]
Turns out there’s no way to vaccinate against or otherwise prevent Dengue Fever beyond long sleeves and mosquito nets, and so the only protection is to not get bitten by its vectoring mosquitos in the first place, but this failure hasn’t stopped the world’s militaries from looking for vaccines against just about everything else.
7.1 – The invisible enemy.
The military’s understandable self-interest in vaccination programs led to the world’s militaries being the first to produce vaccines against multiple diseases: against typhoid by the British Army, and then against streptococcus pneumoniae, adenovirus, rubella, Japanese encephalitis, meningococcal meningitis, hepatitis A, and influenza by the American Military.[v] Influenza perhaps sparked the strongest sense of urgency due to the 1918 Spanish Flu Pandemic, however troops did not begin to receive regular vaccinations until 1945, a prophylactic luxury that the forces stationed in northern France and southern England during the peak of World War I (WWI) would have benefitted from immensely.
It was simultaneously in these two separate regions where military physicians in 1917 begin to notice deaths suddenly occurring from a disease that appeared “influenza in type” whose hallmark was the bluing cyanosis across the lips of the condemned, a symptom that would also begin to appear decades later of victims also meant for meatgrinders powered by the greed of the powerful. In southern England it was Aldershot, the “Home of the British Army” which grew from a small Victorian town to a massive military hub beginning with the Crimean War in the 1850s. By the start of WWI, Aldershot was the British military’s largest base, hosting some 20% of its forces. It was also home to the Cambridge Military Hospital, the first to receive casualties from the Western Front.
In France it was Etaples within the Pas-de-Calais, home to the British Army’s largest hospital complex of over 20,000 beds where doctors simultaneously noticed what appeared to be “almost a small epidemic” of this mysterious extremely deadly disease whose mortality was easily over 40% in those industrially concentrated troops. Eerily similar findings from doctors in both locations were published by the Lancet in 1917, and all indications are that these small endemics were in fact the first nucleations of the 1918 Spanish Flu Pandemic.[vi] So once again, the Pas-de-Calais would host the emergence of a mysterious and highly deadly disease directly connected to coordinated international military activity.
And although this martial etiology may explain the location of that pandemic’s origins, at first glance it does not seem to reveal its exact genome, which seems to have disappeared and has never been isolated in full. However it did leave a signature, and all eight HA genes of today’s H1N1 Influenzas can be traced to a convergence around 1916,[vii] and even more tellingly in 2009 when the H1N1 Avian Flu pandemic began about two-thirds of older persons in America appeared to have immunity from it, thought to be due to the 2009 H1N1 strain already being forgiven by the Original Antigenic Sin suffered from the 1918 Pandemic by those infected, which allowed them to immediately rally bespoke antibodies against their old nemesis, this pandemic virus.
The 1918 influenza carried a novel type of blood-binding protein, or hemagglutinin (HA), resulting in it founding the H1 lineage, and although after burning through humanity and then appearing to dissolve, those who survived it still carried its memory and were far more likely to survive the 2009 H1N1 pandemic. And, of course, it did not completely disappear, but only appeared to diffuse, as its HA genes mutated regularly over the decades following the pandemic.[viii]
Analysis of the regions of the 1918 Spanish Flu’s genome which have been found revealed they appeared more phylogenetically mammalian than avian, indicating a higher level of adaptation to mammals, however all of the empirical evidence points to humans spreading it into swine and not the other way around.[ix] And so decades later, when it was likely passaged and then got out of someone’s laboratory in 1977, the H1N1 Influenza would again be referred to as a “Swine Flu” due to some sort of hypothetical recombination in pigs which no one’s ever actually demonstrated.
But there is another hypothetical barnyard pathway for its emergence which has yet to be explored in the literature, however before it’s reached – there is one final road to cross.
Animal Farm.
8. “To tolerate social conditions that he would otherwise find intolerable.”
Chicken farms saw their first outbreak of what would be identified in 1955 as highly pathogenic avian influenza, HPAI, back in 1878 in Italy, at which point an agricultural Rubicon was crossed - as this “Fowl Plague” would eventually become ubiquitous on poultry farms across the globe, hitchhiking on wild fowl to travel from farm to farm when not transmitted by the commercial trade of poultry itself. It would be noticed on American farms in the 1920s where it was twice eradicated, however as the pace and prevalence of industrial farming spread so too did HPAIs, and a much larger outbreak occurring on American farms beginning in 1983 cost more than $70 million to eradicate and took 17 million avian lives.[i] By 2006 a conference was called to address the fact that their international emergence had increased sharply since the turn of the century compared to the previous 40 years, where they calculated that the impact of avian influenza had increase by 100-fold in the preceding five years compared with the 40 years before that.[ii]
This accelerating threat led to the development of an ingenious vaccination program which inoculated birds heterologously with a vaccine that carried both the HA blood-binding protein genes of the H7-subtype being targeted so that the immune system would target the epitopes carried by that class of virus, but with a different enzyme called neuraminidase (NA) of the tame N1 field-virus meant only to serve as a tracking device for vaccinated chickens. However even with this double-pronged approach, which isn’t mimicked in any human vaccination program, the inherent population density of poultry farms and facile airborne transmissibility of avian influenza has led to the observation that vaccination programs without expansive and concomitant testing programs are entirely impotent in crowded commercial settings.
As it turns out, the artificial population densities of chicken farms and transmissibility of airborne viruses leads to the immunological truism that: “A vaccination campaign which is not managed appropriately is most likely going to result in the virus becoming endemic.” And failing to combine vaccination programs with surveillance and other biosecurity measures leads directly to antigenic drift, and the selection of more virulent variants. Mexico became the posterchild for this practice when practicing vaccination without any other measures since 1994 lead to antigenic variants which escape immune response in the following years.[iii]
Mexican porcine practices would again come under scrutiny in 2009, when that H1N1 pandemic was linked to sketchy practices on Mexican swine farms, for good reason – as you’ll soon find out.
Prior to the 21st century there had only been one documented instance of a HPAI escaping into the wild, when it killed about 1,300 South African common terns.[iv] However as of this writing in 2021, HPAIs have established a pattern of jumping into wildfowl multiple times a year, especially in Asia where China hosts over 40% of the world’s egg-producing chickens and is behind only America in its number of broiler chickens.[v]
8.1 – “You won’t like me when I’m angry.”
And so with increasingly regularity, the avian influenzas ubiquitous to most industrialized poultry farms begin the piecemeal step-by-step process of becoming highly pathogenic, at which point these incredibly lethal HPAIs gain the ability to jump into humans from chickens. When an avian influenza’s genome makes one particular change it becomes designated as “highly pathogenic,” generally gains the ability to infect and kill humans, and gets designated as a potential pandemic pathogen.
But luckily for us, given that just like the 1918 Spanish Flu, the mortality rate from these infections is roughly around half – this process does not happen out of nowhere, and requires several waves of successive infections for the quasispecies mutant swarm of avian influenza to find the mutations which will let it adapt to its new human hosts, and so poultry farms are routinely monitored for this increase in pathogenicity that’s occurring with greater and greater frequency, which is indicated by the insert of four amino-acids within a virus’s spike-protein. There’s a bit more to it than that as well, however the bottom-line is that HPAIs don’t just appear out of nowhere, and require a process of trial-and-error to emerge from poultry farms and noticeably infect humans as highly pathogenic avian influenzas.
The diseases caused by quasispecies mutant swarms may often seem to appear out of nowhere, but careful immunological surveillance of the H7N9 strain of avian flu that first emerged off Chinese poultry farms started back in 2013 has helped reveal the underpinnings of their amorphous nature. As the COVID-19 Pandemic raged so too did the seventh wave of H7N9 Avian Flu across Chinese poultry farms, where it’s infected more than 1,500 people and killed over 600 of them since its quasispecies mutant swarm first began attempting to jump into humans in in 2013.[vi]
During its fifth swarming wave of emergence from the farms scientists noticed that the H7N9 Avian Flu’s genome undergoing all the hallmarks of going from low pathogenicity to high pathogenicity, however unlike other low pathogenicity flu viruses, H7N9 had already demonstrated the ability to infect mammalian hosts as well as birds even before going highly pathogenic, which is usually required to successfully jump between species, and bore the molecular markers of plenty of past mammalian interaction and infections.
This interaction could’ve come over the past decades of endemically infecting farms all across the planet, interacting with small mammals and humans alike, or from other less natural sources, but regardless of how they got there – its clear that the H7N9 Avian Influenza has had extensive past interaction with mammalian hosts, and has been infecting humans since at least 2013 when it was first noticed on poultry farms.[vii]
However during the fifth wave of its emergence, the hallmark of highly-pathogenic influenzas easily able to target humans and many potentially pandemic pathogens emerged: A four amino-acid insert on the strain’s spike-protein. If that sounds familiar it’s because in SARS-CoV-2 this four amino-acid insert is called a “polybasic furin cleavage site,” which an unemployed ex-con and his dad pointed out was the hallmark of serial passage of avian influenza between ferrets during the gain-of-function experiments in 2012, which lead to the moratorium against this particularly dangerous and potentially deadly type of research.
Oddly, the literature covering gain-of-function passage of avian influenza between ferret continually refers to this four amino-acid insert on a spike-protein as a “multibasic” cleavage site, and the majority of the literature covering SARS-CoV-2’s insert referred to it as “polybasic,” making it tough even for someone familiar with the field to make the connection, nonetheless an outsider. And so although SARS-CoV-2 isn’t the only coronavirus with a polybasic furin cleavage site (FCS), the telltale indictor of high pathogenicity that’s found in avian flus only on farms and in labs that’s inserted as a four amino-acid cleavage site for the blood-protein hemagglutinin instead of furin, SARS-CoV-2 is the only one in its family of betacoronaviruses with one, and the only coronaviruses to have one only have at most 60% of their genomes in common with our friendly neighborhood novel coronavirus.
So when the fifth wave of H7N9 Avian Flu, a strain already somewhat acclimated to mammals, sprouted a polybasic four amino-acid insert – the scientific community took a bit of notice. Researchers used extensive testing on ferrets, close cousin to the minks farmed across Europe and North America who like many cousins can interbreed but sometimes have defective offspring, to demonstrate that the polybasic four-base insert imbued this fifth wave of H7N9’s quasispecies swarm with the ability to effectively invade deeply and widely into ferret brains when previous strains couldn’t infect them at all, and also infect eye-balls as well as intestinal tissue for the first time.[viii]
Infecting eyeballs especially isn’t a sign of a natural coronavirus, but it’s another trait shared with SARS-CoV-2, further indicating an unnatural origin.
And although its FCS appears to allow for SARS-CoV-2 to spread almost indiscriminately in the air to host populations of two different species, both humans and farmed mink, the polybasic insert in H7N9 hadn’t yet unlocked the ability for airborne transmission between laboratory ferrets. [ix] So even in a virus already able to transmit by direct contact to some mammals since it first emerged, a polybasic insert alone isn’t the only key that unlocks pandemic airborne transmission into mammals – however it is the key for many strains of avian influenzas, and all highly pathogenic avian influences can transmit on contact to ferrets and guinea pigs.
And in the case of H7N9 it seemed as if the lock had somehow started at least partially turned, since it wasn’t until this fifth-wave and its polybasic-bearing spike-protein that a huge spike in human infections and deaths was noticed after nearly 300 died during that wave, and the alarm was officially sounded despite even the vaguest hint of any human-to-human transmission. [x]
Without looking for it as it’s occurring, it’s impossible to know exactly how the quasispecies mutant swarms of the same virus infecting two species with limited daily interaction leads to increased pathogenicity, but given the underlying unpredictably fractal and quantum nature of how these quasispecies swarms spread it seems reasonable to assert that without looking for the roll these quasispecies swarms are clearly playing, defining their action as waves is going to remain nebulous and imprecise.
And it’s important to keep in mind that this was by no means a natural virus, H7N9 clearly emerged from poultry farms, and yet even in this controlled unnatural setting its sudden spike in infections and mortality during the fifth wave and its emergent polybasic cleavage-site in 2017 was incredibly alarming to scientists. However its unnatural birthplace means that its early extant affinity for mammals is by definition the result of something other than purely natural selection.
H7N9 is by no means a natural virus, it’s clearly the result of poultry farming, and yet it provides a remarkable number of parallels to SARS-CoV-2’s genome. Poultry farms and their issues with highly-pathogenic viruses and vaccination programs seem like a really solid parallel to studying how humanity is dealing with COVID-19.
However this isn’t something the legacy media wants you considering too much, because both situations have one simple answer. And its one that would cost the few dozen people who own America’s media corporation to loose everything they hold dear. Spoiler alert: Your life isn’t one of them.
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8.2 – Lies are the most deadly contagion.
So in latter part of 2019, when an airborne respiratory pathogen with intensely pandemic properties emerged without warning from the city of Wuhan – when there was no sign of the trial-and-error that has accompanied the zoonosis of every other pandemic virus, or potentially pandemic pathogen, ever on earth. Famous and esteemed virologists all across the planet rallied together to tell humanity just how very natural this virus appeared, polybasic cleavage site inserted out of nowhere and immediate human-to-human transmission and all.
But in fact, a serological survey of the city of Wuhan a few years before the pandemic found no evidence whatsoever that anyone had been infected by any SARS-like coronavirus at all.[xi] Beyond lacking any evidence of even a single preemptive wave of infection, even more strangely, as soon as it emerged SARS-CoV-2 was estimated to bind to the human ACE2 (hACE2) receptor some 10-20x more tightly than SAR-CoV did even at the end of its nearly one-year epidemic.
And one of the stranger assertions from the Chinese government and extension the WHO, was that this novel pathogen was having a difficult time accomplishing any human-to-human transmission, tweeting on January 14th 2020 that there was “no clear evidence” of this, and even still on January 22nd 2020, when it is now known SARS-CoV-2 had proliferated from Wuhan to every industrialized nation on earth, the WHO was still insisting that the extent of human-to-human transmission was not yet known.
Perhaps this was because some of the parties involved were a little bit nervous about and well-aware of the truism in pandemic epidemiology, as the British authority on influenza Professor John S. Oxford, recently phrased it: “We appreciate today that a unique characteristic of a pre-pandemic virus lies in its inability to spread from person to person."
Certainly this seems to hold true for avian influenzas we’ve discussed, and although the English Sweat may first seem to violate this assertion, the fact that it was likely a hantavirus vectored by rodents means that it never necessarily had to spread between people, only out of the ubiquitous rodents infesting every English ship and dwelling and into the people living alongside them in a highly pathogenic state.
During the English Sweat, it was as if the ever-present rodent infestations served as poultry farms interwoven into our very civilization. Where we went so did they, and when our populations grew denser and more volatile, so did theirs – and so did the hantaviruses they hosted within them. English rodents co-hosting quasispecies mutant swarms along with their English hosts, eventually acting as furry little fifty-fifty time-and-proximity bombs once their populations grew dense enough to cause the hantaviruses they hosted to go into their highly-pathogenic state.
So without using an immediate animal vector like a rodent or mosquito, the novel coronavirus’s immediate apparent person-to-person spread was one of a long litany of natural expectations violated by SARS-CoV-2 as the COVID-19 Pandemic began, which the virological community rallied to define as natural nearly from the moment it started – quickly condemning any depiction of it as possibly engineered as a “conspiracy theory.”
This sentiment was echoed by nearly every major media outlet on earth, from CNN and MSNBC to Scientific American and the New York Times, and even National Geographic. And a natural origin for the novel coronavirus was embraced by everyone from the directors of the CDC and NIH to the editors of every major American scientific magazine. For whatever reason, it took an unemployed ex-convict whose last formal biological education had been getting a 4 in AP Bio over 20 years earlier,[xii] to write the first peer-reviewed look at a laboratory origin for this novel coronavirus and its concomitant pandemic, guided and assisted by his retired bioinformatician and geneticist father as well as some additional internet help.
And then, almost as paradoxical as the ongoing pandemic itself, this paper was almost entirely ignored by the academic community at large and the legacy media. No one asked why the dozens and dozens of virologists involved with gain-of-function research and collecting many millions of dollars since had failed to published a single article about how gain-of-function research had yet to be ruled-out or even explored at all:
These propaganda efforts have been bolstered by possible collusion from American scientists, some of which is detailed below – but also most notably by one Peter Daszak, who had been publishing papers on coronaviruses alongside the primary Chinese person-of-interest, Zhengli Shi, for years. Perhaps most notably, Daszak is listed as a co-author in the paper first documenting the isolation of a coronavirus from a bat that targets the ACE2 receptor – just like COVID-19 – research done in Wuhan’s virology lab and supervised by Zhengli Shi, and led by a second suspect Chinese researcher who you’ll meet below. At best, Daszak is perhaps acting as an unwitting agent of the Chinese government, but regardless holds an enormous conflict-of-interest. And if nothing else, it is wildly irresponsible to speak-out against the possibility that the virus got out of a lab when a natural origin has not been conclusively demonstrated. Daszak’s statement in The Lancet is either incompetence, or is meant to be a smokescreen for the wanton hubris and greed that have fueled the dual-use or “gain-of-function” research detailed below: As one possible related project which may have overlapped with this one, coronaviruses have been seen as a viable vector for an HIV vaccine for years – a project with hundreds of millions of dollars dangling over it. And unfortunately Daszak is far from alone, there are countless “journalists” mindlessly regurgitating statements from the Chinese government and the WHO with no effort to fact-check whatsoever, as well as “scientists” whose real job is running PR for pharmaceutical and research companies who have spent weeks serving China by making extraordinarily misleading and overconfident statements to the public about the origins and capabilities of this virus. As far back as 2015, Chinese labs were reported to have been involved with dual-use gain-of-function research, mixing and matching viral genomes in the lab, research that accelerated after the Chinese military made a massive push to expand their biotechnological capabilities. And it should be noted that in 2018, the esteemed scientific journal Nature – which has published numerous articles speciously claiming this virus is definitely natural – was revealed to have buckled to censorship demands from the Chinese government, killing over 1,000 articles to placate their Chinese partners.
And then maybe the most ham-fisted and definitely the most unethical part of it all, is the most prominent and heralded scientist-turned-journalist refusing to engage with the paper, implying it never should have been passed peer review at all - even going so far to say people covering the pandemic should put their own personal hunches over formal academic peer review in general. So to figure out why the academic and popular press were both pretending a peer reviewed paper exploring the history of gain-of-function research, especially the serial passage pioneered for vaccine production did not exist at all, and to finally determine the origins and fate of the COVID-19 pandemic, the author kept writing.
FBI
9. The menace of viral shibboleths and the masters of our fate.
Long before he won the Nobel Prize in Economics for their joint work, Daniel Kahneman piled into the back of a military jeep with his best-friend, Amos Tversky, and bounced across a Middle Eastern war zone strewn with landmines, sampling soldiers’ performances and impressions of armed combat while also gathering information about which MREs were preferred by sifting through piles of garbage to find out what wasn’t being eaten, an approach that made newspaper headlines.
After their teeth were chattered by mortared potholes, they were cut on this early scientific sampling of all-too real human behavior, motivated by the overarching idea that our actions are often quite different from what raw economic theory posits they should be in any given situation. One of their early findings was that soldiers in war-zones do not seem to be fighting for the abstract ideals they are often touted to be defending. When it comes down to it each man is fighting for the friends beside him – the first scientific quantification of military squads as bands of brothers.
In the decades that followed, Kahneman and Tversky would make countless contributions to our understanding of human group-behavior and decision-making. One of their earliest discoveries was the availability heuristic, the inevitable tendency for our judgment to be influenced by how easily examples of a given topic come to mind. For instance, media coverage of the fatalities makes tornadoes seem more dangerous than asthma and lightning deadlier than botulism, even though those medical risks respectively kill twenty and fifty-two times more people than the natural disaster they were just paired with.
Their experiments which subtly prime participants with anything from financial terms to Monopoly money stacked on the table do make people spend twice as long trying to solve a tough problem instead of giving up on it and show more self-reliance, however they also became more selfish and less helpful to someone in need. And placing a banner with watchful eyes on it above an office “honesty box” designated to take payments for caffeinated drinks will make donations spike significantly when compared to a banner with festive flowers on it being hung – great if you are collecting the money, costly if you are giving it.
And they demonstrated that those exposed to possible sources of contagion will be harsher when evaluating behavior that is not undoubtedly immoral but just does not sit right, and more negatively judge a man who, for instance, fornicates on his grandmother’s bed – not while she is watching, just while housesitting for her. After disgust has been elicited subjects become “more likely to endorse biblical truth than those not subjected to the polluted air.” Placing someone next to a hand-sanitizer dispenser will make their moral, fiscal, and social opinions more conservative.
And this phenomenon applies directly to our criminal-justice system as well, as “a study of people serving as mock jurors found that those highly prone to disgust were most inclined to judge ambiguous evidence as proof of criminal wrongdoing, to impose stiffer sentences, and to see the suspect as wicked.” But maybe most disconcertingly, this same study was also replicated with law students, police cadets, and veteran forensic experts. Turns out judicial punishment might have a lot more to do with hunches and biases than any sort of legal philosophy than we might want to admit.
There’s even a theory that culture itself and all the behaviors it encompasses “originated as a behavioral adaptation to an epidemic-filled past.” So from spicing our foods to showing affection to burying the dead – there may not be a single culture touchstone left unmarred by immunology’s influence. And these immune behaviors “once developed, stick around because the people who indulge in them are less vulnerable to infectious diseases. The behaviors, passed down through the generations, become entrenched.”
And it’s this interplay between culture and disease which earlier answered our first mystery, and can be used as the first thread to untangle another immunological Gordian knot: How did the 1918 Spanish Flu Pandemic start and where did it go?
9.1 – Getting by with a little help from their friends.
Despite an enormous amount of disparity across the globe in terms of public health precautions in the midst of the COVID-19 Pandemic, the annual cycle of seasonal influenza failed to flare up at all during the 2020-2021 season. A decline was anticipated due to the general implementation of some kind of public safety measures internationally, however instead of declining at anything resembling a linear rate, the seasonal influenza seemingly didn’t materialize at all in much of the world – those struck hard by COVID-19 and those that managed to avoid the worst alike.
It was as if the seasonal flu evaporated, since that’s what functionally happened as the quasispecies mutant swarms which had spent decades slowly adapting alongside us and following the same rhythmic pattern were suddenly denied the full extent of their predictable refuge of annual winter congregational spaces. And so the more virulent variants which only emerge after transmission between more and more hosts never occurred, and a weakened quasispecies swarm just got passed around mostly asymptomatically, without the chance to gather enough variants together long enough to become really virulent.
So the sudden and instantaneous disappearance of the virulent examples of seasonal flu’s quasispecies mutant swarms occurred when the usually cycle of human interaction set a steady rate of change in transmission opportunities that the seasonal flu adapted to year in and year out, chances which were suddenly dispersed in 2020.
Seasonal influenza simply thinks it didn’t get a winter this time around, and is patiently and often asymptotically waiting in quasispecies swarms too weak to do much other than maybe weakly jump to a close family member here and there and spread weakly around movie theaters out of one or two hosts instead of the several dozen required for an endemic to begin. However when human population densities return to what they were in the winter seasons, it will flare right back up if the current public health measures are abandoned.
And so just as populations that are too diffuse make it impossible for quasispecies mutant swarms to create enough immunological heat to do anything than lay dormant, the opposite of that effect also holds true. So in the lead up to the War to End all Wars, when humanity began to organize itself in populations which grew denser and denser and never stopped shifting past each other as troops were massed and then transferred, and the rest of the martial industrial machinery of farms and factories hosted crowded populations all swarming around each other in a mass of humanity that grew denser and denser – eventually there was enough immunological friction and something began again at the Pas-de-Calais, where the English Sweat had followed its soldiers eerily across the Channel to France, rapidly extinguishing their lives while leaving everyone else around them unscathed.
However we now know that the English Sweat wasn’t caused by some mysterious vapor, rather it was likely the highly pathogenic state of a hantavirus strain, jumping in its white-hot virulent form out of the rodent hosts that’d burrowed themselves ubiquitously into our civilization, with the same signature coin-flipping Thanos-esque snap of lethal pathogenicity as the a highly pathogenic strain of influenza burning across a poultry farm. But since the men gathered together by military and industry all shared their beds with rodents, all of them subject to the same risks as workers on a poultry farm.
And so when the English Sweat’s hantavirus strain went highly pathogenic it wasn’t interacting with hosts whose immune systems it’d never encountered before – due to their constant and unavoidable interaction with rodents, these men would’ve already been hosting the partially formed quasispecies mutant swarms that create the highly combustible immunological states necessary for highly pathogenic strains to ignite: Quasispecies mutant swarms with a wide mix of variants, indicating a swarm has already gained the ability to reach multiple organ systems, as well as high MOIs, since more fuel always makes for a hotter fire.
With the English Sweat it was the soldiers and monks and other men gathered together by industrialization who interacted enough with rodents to allow for volatile quasispecies clouds to build up within them, with the 1918 Spanish Flu Pandemic no intermediate host was necessary. By then the complexity of our civilization had allowed for enough population density to make humans the mice this time around, because influenza was airborne and transmitted relatively easily between hosts in crowded rooms, so an intermediate host was no longer needed as it was for a hantavirus to infect humans.
And so at Aldershot and again at the Pas-de-Calais where the English Sweat had previously found a home, when the martial and industrial population density and volatility increased the number of transmission events enough, the quasispecies mutant swarms followed ancient evolutionary pathways and committed the most forbidden type of Original Antigenic Sin: Murdering their hosts as they become highly pathogenic – a Sin that grants it the possibility of jumping into a new host species. Nothing comes without its price.
Jumping into its highly-pathogenic state among the men packed like barnyard animals into military and industrial settings, the H1N1 Longpig Flu would soon leave its original host and jump into pigs as well.
The pathways for this highly-pathogenic species-jumping state were likely lain in times of famine when a host population’s density would be artificially reduced because of a loss of numbers, so RNA viruses evolved to go highly pathogenic states in an attempt to host-switch into a new home. Which is another telltale sign that the 1918 Spanish Flu was the result of humanity turning itself into a barnyard as far as influenza transmission is concerned, functionally into diseased rodents infesting our own war-machine, and causing our endemic human influenza to “think” it needed to attempt to find a new host, going highly pathogenic to do so and successfully jumping from humans into pigs.
There’s no longer any doubt about the direction of transmission, and its Sin was probably worth it as far as the 1918 H1N1 Longpig Flu was concerned since it no longer has to rely on humans as its sole host, and happily infects swine as well as the other, other white meat all across the planet.
As another clue to its origins, not only did the 1918 H1N1 Longpig Spanish Flu Pandemic kill roughly half of its host population – primarily the densely packed young men that War turns into fodder of one kind or another whose proximity allowed them to all become one interconnected immunocompromised patient with a volatile quasispecies swarm just waiting for a spark – its quasispecies mutant swarms also gained the ability to host-switch and jump into a new porcine species, another hallmark of the emergence of a highly pathogenic strain of RNA virus and the only time it’s been definitively observed. Since unlike regular avian influenza strains, not only can HPAIs infect humans, they can infect guinea pigs and ferrets upon direct contact as well.[i]
Oddly, not a single American legacy media outlet linked the COVID-19 outbreaks on mink farms across multiple continents to the fact they’re an overlapping species with the lab ferrets especially used in the vaccinee-related gain-of-function experiments which lead to a moratorium against the practice in 2014. Certainly, the dire economic circumstances of American journalism overall and the absurd amounts of money pharmaceutical and defense companies stand to make from gain-of-function research has nothing at all to do with this comically willful blindspot, as American journalists happily stenograph away and write only what the people who own them allow them to write.
So brave to mention the need for an actual investigation instead what would’ve been a farce even if it’d happened a year earlier, while refusing to link to the peer-reviewed research that demonstrates COVID-19 is almost certainly engineered, and probably linked to one vaccine program or another like many other puzzling outbreaks in human history.
And if it still seems implausible that the 1918 H1N1 Longpig Flu was in fact the first international instance of a human influenza going highly pathogenic, there’s one last memento to examine. After the Spanish Flu burnt through a host, it left the same cyanotic blue kiss on human lips as it does chicken wattles today – as if all the oxygen had suddenly been sucked out of its hosts by a backdraft.
Pitch Black.
10. “When you know about something it stops being a nightmare.”
Probably the first moment I didn’t feel like a complete child, like the adult world had started to beckon, was when my dad sat me down to talk to me about keeping an eye out for any mail that didn’t look quite right.
Maybe it would be lumpy, or seem to be stained, and definitely keep away if there were any noticeable wires. So I dutifully inspected every package I found on our porch, a little bit nervous each time I just picked one up before I could fully inspect it – scared for a moment that it might blow up in my face. But luckily for our family, the Unabomber never chose to target my dad. But during the years that the case’s momentum grew in the media leading up to the publication of his Manifesto when I was about 12 years old, each and every holiday season seemed like more and more of a risk.
And yet actually reading the Unabomber Manifesto made me relax a bit, since although my dad’s career applying his PhD in microbiology to the design of genetic databases and other related bioinformatic pursuits seemed tangential to the hyper-industrialization that Kaczynski was warning about, I remember feeling reassured that my dad’s quiet career as a federal civil servant probably hadn’t put him in the line of fire.
Although he never mentions it by name, Kaczynski was obviously aware of the Asilomar Conference on Recombinant DNA in 1975 and started his bombing campaign a few years after it. Asilomar was assembled after Paul Berg had already attached the DNA from a carcinogenic monkey-virus named SV40 to the DNA from bacteria-infecting virus, making a chimeric Frankenvirus which he was then contemplating sticking into some E. coli bacteria, whose close cousins had no problem replicating within and spreading among humans.
Luckily for humanity, at least for the time being, the experiment was paused since the monkey-virus involved was already known to cause tumors in mice, and although the exact strain of E. coli that Berg was using wasn’t known to be able to infect humans, the scientific community at-large agreed to halt this type of genetic engineering until some guidelines could be agreed upon.
Most of the guidelines were around the practical considerations that would go into containing different types of pathogens and toxins, and the conference set the stage for what has becomes the Biosafety Level system, highlighted as the entire world learned that Wuhan’s WIV was the only BSL-4 lab in all of China.
10.1 – Fixing what isn’t broke.
Berg’s prospective experiment attracted so much attention back in the seventies in part because it was taking place at the famous center of vaccine research, the Salk Institute – whose founder had created the first polio vaccine, which was inactivated unlike Sabin’s live-attenuated OPV vaccine. Sabin’s OPV vaccine proved more effective than Salk’s and was used to put the final nail in polio’s coffin, that is until the past few years when OPV has demonstrated it’s V-1000 ability to reassemble itself into its fully virulent paralytic form. However one particular group of people was very interested in Berg’s experiments being concluded, since that exact same monkey virus, SV40, was contaminating strains of both the live-attenuated OPV vaccines as well as the inactived polio vaccine, during the serial passage necessary for vaccine creation, and they wanted a fix.[i]
Perhaps it’s a good time to point out that HIV, which began to emerge in the early 1950s, has never been confirmed as a natural zoonotic event,[ii] and there’s been long-standing speculation that its emergence was due to a batch of experimental polio OPV vaccines known as CHAT gone wrong.[iii]
This was almost 20 years before Asilomar and the technology that would allow for the kind of recombination Berg wanted to do, an experiment likely at least partially driven by financial motivations, since there was nothing at all wrong with Sabin’s original OPV vaccine, but someone wanted to try and play a bit of god and create a new vaccine that actually wasn’t epidemiologically needed and might lead to a patent or a few sales.
And the theory that HIV was seeded by an improperly prepared batch of the experimental CHAT-OPV vaccine recently outcompeted five other possible scenarios in a complex statistical computer simulation: Since the earliest 68% of AIDS cases and 76% of HIV that emerged in Africa and so presumably the world emerged in the villages where the experimental CHAT-OPV administered was passaged through cells isolated from African chimpanzees known to host SIV – nominally considered to be HIV’s parent virus – instead of the SIV-free Asian macaque cells used for serial passage and vaccine production in the rest of the world.[iv]
The argument that HIV’s emergence wasn’t entirely natural was bolstered by another study, which looked at the amount of genetic distance between HIV’s putative ancestor, SIV, and especially noting the extraordinarily low odds of the four transitional mutations that were needed all occurring within one host, also suggest human involvement playing a role in HIV’s emergence. Instead of contaminated CHAT-OPV batches, they suggest that the accidental serial passage of SIV-infected cells between random patients that was amplified by the widespread use of unsterilized needles throughout Africa in the 1950s.[v]
It’s unlikely to be a debate that’ll ever be settled as there’s fundamental disagreements about which vaccine batches were passaged where,[vi] but regardless of whether the recombination that led to HIV happened naturally due to some hopefully intoxicated interspecies experimentation, or because of an improperly processed batch of OPV vaccines passaged through simian cells with SIV and left unexposed to the protein-cleaving enzyme meant to deactivate any latent viruses – the fact of the matter is that an improperly prepared batch of an experimental and entirely unnecessary live-attenuated OPV vaccine may well have sparked the ongoing global AIDS pandemic, which has extinguished 40 million lives and counting since it started.
And it’s pretty hard to imagine it’s a coincidence that an experimental an unnecessary new vaccine was being tried out in the third world, in the geopolitical middle-of-nowhere. Because so what if something went wrong, it’s just a bunch of African villagers – what recourse could they possibly have if they were harmed by CHAT-OPV?
But at least many years later at the Asilomar Conference in 1975, they proactively agreed not to do any sort of recombinant engineering involving DNA from highly pathogenic genomes and tried to control the scale of any dangerous experimentation. Unfortunately, if only took about two years for the H1N1 Longpig Flu to be engineered, presumably by serial passage during vaccine work, and then leak out of what was almost certainly a military laboratory.
And it probably wasn’t the last time for that particular strain either, despite the fact that no one’s ever taken responsibility for either. Funny how that works with lab leaks.
10.2 – Sick little piggies.
Since the H1N1 strain that emerged in 2009 and caused that year’s nominal “Swine Flu Pandemic” also had a highly irregular genome. Instead of two regions separated by a temporal gap, something functionally impossible to explain without laboratory involvement, the 2009 H1N1 Longpig Flu strain had three distinct genes representing three very distant regions of the world, not known to have their H1N1 strains intermingle at all.
The theory was that the nature of global trade had somehow lead to a strain that was the product of genes involving three distant countries, and at least two recombination events creating two viruses both of which would’ve had to escape disease surveillance attempts. However this pandemic began with just a single introduction in Mexico, long known for its irresponsible porcine vaccination practices, and all three genes had actually been sampled separately over a decade ago. And so the likelihood of another vaccine serial passage mistake triggering a human pandemic again appears extremely high.[vii]
Oh and speaking of lab mistakes and mysterious diseases which seem to appear out of nowhere with sketchy human-to-human transmission, it might come as a surprise to learn that neither SARS-CoV nor MERS-CoV were ever officially demonstrated to be zoonoses either, and both might also be laboratory leaks. Although SARS was linked to civets and MERS camels, neither population of farmed animal was ever demonstrated to be a reservoir of either virus, nor to have first passed either virus into humans in the first place.
Civets and other small carnivores were found infected with SARS, however humans appear to have given it to them in all cases.[viii] And in the case of MERS, its initial outbreak was said to definitively originate from a single molecular source, however in many early cases there was no history of contact with camels or anyone who could’ve been infected at all.[ix]
Plus MERS-CoV’s supposed molecular link to nature was incredibly scant: One single sample from a batch that might’ve been later accidentally thawed taken from one lonely bat was the only place the “matching” region of base-pairs was ever found,[x] that is why you probably thought MERS “came from camels.” But because the world was reassured by Dr. Ian Lipkin,[xi] who would later be one of the five co-authors of the most logically convoluted, scientifically vapid, and lethally misleading science paper ever published, The proximal origins of SARS-CoV-2, which speciously and erroneously claimed to demonstrate that the COVID-19 Pandemic was almost certainly the result of a natural zoonosis, everyone had believed him that MERS-CoV was as well.
And Dr. Lipkin then implied that the people doubting him or calling his judgement or ethics or ties to the kind of gain-of-function research which could’ve created MERS-CoV in a lab were just jealous of his unabashed and undeniable genius.
But because such a limited number of people died and most countries were left entirely unaffected, the general public shrugged after both of those outbreaks, went back to whatever daily regime of prescription medications most in the West are on, and almost entirely went along with the narrative that the COVID-19 Pandemic was the product of a natural zoonosis throughout the entire first year of its existence – SARS and MERS had been, so what’s one more!? Gain-of-function research linked to vaccine development? Serial passage through lab ferrets which could imbue an affinity to farmed mink as well and lead to the world’s first simultaneous interspecies pandemic, what was all that about?
Our legacy media throughout 2020 and into 2021 still hasn’t wanted you to know, since unfortunately if journalism is printing what someone else doesn’t wanted printed – nearly everything passing today as “journalism” is just fancy stenography for the billionaires who in addition to literally owning the media, also own controlling interests in vaccine companies and the defense industry.
Your families might die or be crippled by debilitating syndromes, but as long as there are enough of us left to keep pumping out the suffering they distill down and sip on their yachts and rockets – “What do you say Jeff, is it bit too oaky this year? Or maybe a touch too much despair on the finish?” – nothing will change and your idea of Truth will be exactly what they allow it to be.
Because of course it wasn’t anyone in the Koch’s family intention for their hundreds of millions of dollars of political manipulation to create any sort of unrest of social tension, these things just happen right? Of course it’s only been with the best of intentions that “philanthropic” families like the Kochs and Sacklers and Murdochs have turned our politics, medicine, and media into their personal playthings.
But it wasn’t always this way, with wealth concentrated into such an extent that a few dozen people can sit back and pull America’s political, medical, and media strings while most of the country competes to see who’s the most free beneath their six-figures of credit card debt and constant lower-back pain. Back in the 1970s though, scientists were worried enough about fallout from Watergate and the corruption it exposed to go out of their way to transparently and openly regulate themselves as best as they possibly could.
In part, to ensure that no one could be accused of a cover-up.
So although way back in lead-up to 1975, Berg wasn’t using the same monkey-virus which may have accidently been mixed into a batch of OPV finalized in just the region of Africa where HIV first emerged, his desire to do experimental work involving vaccines, interspecies viruses, and human DNA first presented the scientific community with the threat that splicing virulent animal viruses into live-attenuated vaccines might pose, since it was impossible to predict exactly how they’d interact with our genome.
Given all these dangers, and considering that there was no reason to tinker with the perfectly good polio vaccines, the scientific community decided at Asilomar never to clone recombinant nucleotides from highly pathogenic organisms, nor with genes involving the production of toxins, nor experiments with recombinant nucleotides meant to be implemented at large scales in a commercial fashion.
Unfortunately for humanity, our Ivory Towers have become Ivory Whorehouses, tenured by those who’d pimp their graduate students and research facilities out to whichever pharmaceutical or defense company is paying the most, and loan-sharking their undergraduates for money used to fund fancy banquets and awards ceremonies – ensuring the next round of funding and donations.
Since beyond UNC’s stonewalling and refusal to release data which could quite literally save tens of millions of lives, Harvard, MIT, and Johns Hopkins have all been contacted about the unethical behavior of researchers representing them – behavior that is also endangering human life by attempting to pull attention away from the reality of just how obviously engineered this virus is.
But none of those institutions care about the possible public health consequences of the lies told with their names on them, the only people they listen to are the ones aligned with their financiers – the philanthropists who want to wear altruism like a peacock’s tail, providing nothing to society except hedonism as they flaunt their inherent superiority over the rest of us.
The “philanthropists” who’ve spent the past few decades trying to make Americans feel grateful for their systematic financial and political cannibalization of our country behind the guises of their false causes are now seeking to alter the human genome directly, using con-men in slick suits to write books about just how joyous this Brave New World will be and appearing on our television to assure us not to worry, that very rich and smart people without any relevant degrees are going to get to the bottom of this pandemic, trust the rich people who want to begin directly altering the human genome far more than has ever been done before – it’ll all be fine. But when this asinine propaganda can’t even get past Amazon reviewers, odds are there’s still a little hope for the rest of us.
So it took until about the turn of the century for research science as a whole to apparently forget about Asilomar entirely, and when enough money was on the table a few billionaires and several dozen research scientists decided it was time for the rest of us to hold their beers while they played God.
11. “The greatest trick the Devil ever pulled…”
On a brisk Thursday afternoon, the former head of Harvard’s Chemistry Department, Dr. Charles Lieber, strode out of a Boston federal courthouse after agreeing to pay a $1 million cash bond, surrender his and his wife’s passports, and disclose any foreign bank accounts.[i]
Lieber had been arrested by the FBI just two days early on January 28th, 2020, on charges that he’d made false statements to Department of Defense and Harvard investigators looking into his ongoing ties with the CCP’s Ten Thousand Talents program, including collaboration with ongoing projects in Wuhan and collecting millions of dollars from the Chinese government for his assistance.
In the early weeks of the pandemic this story certainly registered, but not nearly as much as something like Zero Hedge being kicked off Twitter for directly tying the Chinese military to the Wuhan Institute of Virology, and potentially the genesis of the COVID-19 Pandemic. Lieber would appear in court again in June 2020 to be indicted on making false statements regarding ties to the Wuhan University of Technology as well as getting paid for his participation with the CCP’s Ten Thousand Talents program, aimed at infiltrating and influencing American educational institutions.
In the confusion around the pandemic’s emergence, the arrest of a Harvard chemistry professor with loose ties to the city of Wuhan certainly seemed strange, but it didn’t seem to have any direct involvement. When samples of SARS-CoV-2 where first being released to the world they seemed remarkably similar, and given how much they spread over the wet market, certainly didn’t seem to be hiding or hard to detect. And so a professor who’d pioneered research into using electromagnetic fields and nontechnology to simultaneously detect individual viruses[ii] getting arrested appeared likely to be coincidental.
At the time of its creation in 2004, Lieber marketed the nanotechnology as an invaluable tool for the military to detect biological weapons,[iii] and in the years that followed it was presumably privatized and patented since this virus-detecting nanotechnology and Dr. Charles Lieber both just about disappear from the internet until his arrest in January 2020.
So there’s no way of knowing exactly how fine-tuned Lieber’s nanotechnology became in the fifteen years since before the COVID-19 Pandemic began, when it was first announced in 2004 it only mentioned being able to distinguish between different families of virus – such as influenza or adenovirus, H1N1 or Dengue Fever – however in all that time, it seems plausible that it was refined to be able to detect even between different classes of influenza strains. And from looking at one of the patents, it sure seems like it’d advanced to the point to be able to remotely detect individual nucleotide variations.
Or maybe it’s even been tuned so well that it’s able to quickly able to detect the full composition of a SARS-CoV-2 quasispecies swarm within any given space, giving anyone with this technology an enormous advantage when it comes to combating and controlling the COVID-19 Pandemic. It’s hard to imagine that the CCP is unaware of the quasispecies mutant swarm phenomenon, since it’s the best explanation for why they’ve been so insistent on collecting fecal samples from absolutely everyone, focusing at first on children, since fecal swabs show far more of the full quasispecies array than a nasal-swab, or than any other common method of collection.
And it helps explain the strange behavior of the PLA, the Chinese Military, in the first several weeks of a pandemic that was killing thousands of its citizens while it stood back and watched.
11.1 – “The strong man who has known power all his life, may lose respect for that power...”
There was nothing apparent on the ground in Wuhan that triggered the secretive military unit which took over the WIV on January 24th, the only notable precursor is that their take-over was a few days after the infamous Batwoman, Zhengli Shi, submitted the paper which disclosed the existence of the RaTG13’s genome to the world for the first time.[iv]
So it wasn’t until several weeks after the “official” start of the pandemic in early December that the PLA sent anyone into Wuhan at all, and it wasn’t as a result of anything logistical or medical – they seemed to be reacting to a paper being submitted to a scientific journal. And we now know that the pandemic appeared to have been raging in Wuhan at least throughout November, and that the December start date is extremely loose at best.
At the time there didn’t seem to be anything exceptional about the data in that paper submitted by Shi on January 20th 2020, until a few weeks later when an anonymous internet user NerdHasPower published an examination of an important genomic ratio used for tracking evolution.
This ratio is called dN/dS and measures whether or not change in an amino acid changes the final protein, and is supposed to end up at roughly 5:1. And it although it eventually gets there when it’s compared between SARS-CoV-2 and RaTG13 – instead of a smooth natural pattern, there’s a distinctively flattened one with sharp steps. And as a formal peer-reviewed analysis would later confirm: The dN/dS ratio between an original strain of SARS-CoV-2 and RaTG13 is the lowest ever found, suggesting “evolution under stringent selective pressure.”[v]
Perhaps like maybe inside a laboratory, given that the dN/dS ratio difference in the spike-proteins of our novel coronavirus and RaTG13 is nearly three-times higher than what was found comparing two definitively natural viruses. And when comparing any other two viruses thought to have jumped between species, when any two assumed interspecies cousin viruses were compared, this ratio only ever managed to get a bit above half of the much higher level found between SARS-CoV-2 and its nominal ancestor.[vi]
And keep in mind that RaTG13 was eventually revealed to supposedly only be a “consensus sequence” from a pool of viruses, speculation began that it was merely a keyboard virus – fabricated to provide a fake “natural” link, so that SARS-CoV-2 didn’t look entirely unnatural.
However there’s another explanation for the unnatural presentation of this ratio, which is probably also why one of the co-founders of the Broad Institute, Stuart Schreiber, organized a letter meant to rally support for poor downtrodden Dr. Lieber.[vii] Whose only crime was allegedly secretly accepting millions and millions of dollars from an adversarial foreign government with an extremely questionable past of unethical genetic experimentation, and which is almost openly committing genocide of an ethnic minority.
Apparently the co-founder of the Broad Institute wants his good buddy Chuck back on Harvard’s payroll and reinstated, since if the Department of Justice keeps being mean to preeminent American scientists who secretly accept millions of dollars for forwarding the interests of a foreign government and then lying about it – other American scientists might not collaborate with Chinese scientists. And if other American scientists aren’t accepting bribes from the CCP, how is the Broad Institute ever going to make sure its brand-new program which just got a $32 million grant from DARPA is able to carry-out the gain-of-function research it has planned if there’s another moratorium?
Although none of its copy mentions manipulating viruses by name, the Foundry makes it very clear that tinkering with the human genome is a priority – nominally to improve it of course – however with fully 10% of the human genome derived from one virus or another,[viii] including a gene that appears to be fundamentally involved with memory which uses a virus-like action,[ix] the idea that the full gamut of experiments on the human genome can be run without being able to serially passage viruses is absurd.
Of course the hyper-rich intent on living as pleasurably and long as possible want full access to do as much as possible with DNA, they’ve earned the right – haven’t they? What the fuck was the Asilomar Conference, isn’t everyone aware of Dr. Ralph Baric’s limitless genius? What’s a FOIA?
11.2 – Maybe universities shouldn’t be built with slave labor?
So perhaps it’s not a coincidence that out of the WHO’s list of 32 candidate vaccines against the original SARS-CoV, only two of them are live-attenuated viruses – and both were being researched at one facility on the entire planet: the University of North Carolina,[x] home to Dr. Ralph Baric, coronavirus-wrangler extraordinaire – who earlier assured the world in an interview with the Italian press that the answers to the COVID-19 Pandemic would be found within the Wuhan Institute of Virology.
Almost like he wanted us looking away from something else.
And oddly, UNC has been home to some particularly hungry lab mice, as starting in August of 2015, right as Dr. Baric was mastering the creation chimeric SARS-like coronaviruses in the lab – the kind of thing you might want as a template for a live-attenuated vaccine, since attempts to make a LAV for Yellow Fever had proved impossible without recombinant chimeric viruses[xi] – there was a series of possible laboratory exposures involving lab workers and “SARS-associated” coronaviruses. All of which came after Baric pushed to keep gain-of-function work on these viruses open, arguing about how much potential good it might do, and how safe these studies were.
Since the WHO and its billionaire-backers have been pushing scientists to develop a vaccine that could cover the entire class of SARS-like viruses since they first emerged:
“For example, if a candidate vaccine against Middle East respiratory syndrome could be tested against hundreds of near relatives of that same syndrome, vaccines that have broader prevention capacity could be selected and rolled out to provide better protection against future emergence of this syndrome. This approach could enhance biotechnological efforts to move from single-virus countermeasures to ones that target a whole family of viruses.”[xii]
But despite this ongoing research into a live-attenuated vaccine for SARS-live viruses, mice running loose and biting workers, vials containing viruses breaking, and equipment lapses – UNC was never concerned about the transmission of a virulent virus and hasn’t felt the need to disclose any of the genomes involved to the scientific community at large, claiming they’ve done their due diligence.[xiii]
And so despite FOIAs by USRTK and White Coat Waste and various other journalists, Baric and the NIH have stonewalled any disclosures about his past research’s possible relationship to the ongoing pandemic behind a supposed “ongoing investigation” which won’t allow them to divulge anything else. Sort of like when the press is demanding to see your taxes, but you refuse to hand them over, claiming you’re under audit – since someone who’s possibly an assert of various entities like Baric would likely feel like he could trick each agency to be concerned about stepping on each others’ toes, and not ever actually insist upon seeing the data that matters.
Seems strange that the scientist who lead the team which pioneered using serial passage and successively higher percentages of human DNA to allow a virus to transition from bat cells to human cells[xiv] would be able to keep all of his files hidden from the journalists requesting it via FOIA, given that our tax dollars paid for it.
Especially considering that after first graying all the rules of the Asilomar Conference, Baric effectively threw them out the window with the publication and utilization of the No See ‘Em molecular technology that would allow nucleotides from a virus at all to be inserted into mammalian DNA without leaving a trace, pioneered way back in 2002 when they used the hepatitis virus.[xv]
And since UNC was the only place on the entire planet attempting to make a live-attenuated SARS-vaccine, it’s hard to imagine those accidents had nothing to do with the ongoing pandemic, especially since their reports seem to be describing a virus that isn’t expected to be infective nor dangerous – exactly what you’d expect from a live-attenuated vaccine strain, not enough of a quasispecies swarm for transmission or significant symptoms. Which also fits COVID-19’s presentation in some cases, in that many people can test positive for it without ever having been even the least bit symptomatic.
This fundamentally alien ability for SARS-CoV-2 to spread so incredibly asymptomatically caused many people to draw lines to what was a supposedly a vaping-induced disease, EVALI, which appeared across America in the fall before the nominal start of the pandemic in December of 2019. It’s a connection that seems pretty tenuous at first, and yet it’s not like there wasn’t anything in the air around the Pas-de-Calais that’s made it such a notable pathogenic birthplace – it simply happened to be where the most humanity happened to get concentrated during military activity.
Which brings us back to the Wuhan Military Games of October 2019.
11.3 – Threading the Eye of the Needle.
As the pandemic unfolded in Wuhan over the coming months, the Chinese Army seemed to be frozen and that the “PLA’s relative lack of response is even more puzzling given that Wuhan is home to major military units that should be capable of deploying to a contingency.”
Much like Aldershot, or Pas-de-Calais with its additional industrial base, Wuhan is an obvious place for the quasispecies mutant swarm from a live-attenuated SARS-like orally-administered vaccine given to PLA troops to first coalesce, especially in the midst of something like their Military Games with all of the additional movement and contact and crowded conditions from one-quarter million extra people being brought in all at once.
So despite all of the CCP’s recent touting about its military capacity, and realizing the pandemic was severe enough to warrant locking down 50 million people once it really got going in January, the PLA seemed terrified of setting foot back in Wuhan and didn’t show up until January 24th, a few days after the Batwoman submitted RaTG13’s consensus genome, and even then it was just three small medical teams of 450 personnel total:
The PLA’s relative lack of response is even more puzzling given that Wuhan is home to major military units that should be capable of deploying to a contingency. These include the Joint Logistics Support Base, notionally the center of the PLA Logistic Support Force’s network of warehouses and stockpiles. According to China's 2019 defense white paper, the PLA Joint Logistic Support Force "comprises the support forces for inventory and warehousing, medical services, transport, force projection, oil pipelines, engineering and construction management, reserve assets management, and procurement."[xvi]
Sure seems like the army had no intention of concentrating itself anywhere near Wuhan again anytime soon, despite having just hosted its Military Games there, bringing in nearly 250,000 citizens from across China to help. Even more odd, is that right before those Military Games, the Hubei Provincial Health Committee simulated an outbreak of MERS-CoV, so they should’ve been well-prepared for the actual outbreak of a pandemic.[xvii]
So perhaps the PLA had taken these Games as an opportunity to test an orally-administered SARS-related live-attenuated vaccine derived from the chimeras originally made at UNC and their own LAV vaccine work, or maybe an oral one given much earlier had simply deattenuated much faster than expected given the artificial population density of Wuhan’s Military Games, which surged right at the phylogenetically-estimated start of the outbreak in October.
Perhaps not incidentally, the Wuhan Military games in fact ran almost concurrently with Event 201, the eerily prescient conference sponsored by the World Economic Forum, The Bill & Melinda (still?) Gates Foundation, as well as Johns Hopkins - all of which have been entangled with some combination of making billions of dollars from vaccines or the defense research next-door to it.
And there may have been one final molecular trigger: Just as strains of influenza can spontaneously gain a FCS after serial passage through laboratory ferrets, instantaneously jumping from a virus that spreads only through direct-contact to one that’s airborne - this exact same process may well have given SARS-CoV-2 its FCS as well, except serially passaging among humans instead of laboratory ferrets.
Recombination with viruses already within a host is one possible way for a virus to appear to gain a four amino-acid insertion like a FCS seemingly out of nowhere, and since humans have loads of endogenous viruses, and when crowded together in an urban setting aren’t functionally all that different than ferrets crowded together in a laboratory cage.
It would be a nice bit of historical parallelism for the COVID-19 Pandemic to have been sparked by the same phenomenon that worried scientists so much back in 2012 during the exact gain-of-function experiments which led to an international moratorium against the practice: The sudden appearance of a FCS after serial passage, and the concomitant airborne transmission it enables.
And there’s actually a very straightforward path for this to happen in a human population: Since SARS-CoV-2’s FCS falls-off when it’s placed back in Vero cells, and the ubiquitous human common-cold coronavirus OC43 already has an FCS nearly identical to the one we’re dealing with - recombination and selection leading to the extraordinarily adaptive FCS getting tacked-on to our novel coronavirus would’ve been a matter of when, not if.
Scientists watched this sudden airborne molecular magic happen among ferrets in the lab, knew how dangerous the implications were, and then enacted a ban on gain-of-function research as a result. Until the temptation to play a little bit more god became too much, and the checks got just a little too big.
And just as the 1977 Longpig Flu endemic was the result of a virus altered by serial passage almost certainly in the attempt to design a live-attenuated military vaccine, an outbreak that served for decades in the literature as a warning against viral gain-of-function research since the risks involved were simply too high - so too was our ongoing COVID-19 Pandemic sparked by a live-attenuated military vaccine program gone-wrong, that was subsequently covered-up by a Communist nation.
After all, as the godfather of gain-of-function ferret-work himself Ron Fouchier noted rather presciently in July of 2019:
“That’s what happened in the 70s, people were trying to do live-attenuated vaccines and do human challenge studies and that might be the way the H1 re-emerged in the 70s. Some people say it was a lab accident. I don’t believe that. I think it was actually human challenge studies and live-attenuated vaccines that reverted that are the likely candidates of the 1970 reemergence of H1. And we need to make sure that doesn’t happen again.”
Because although the PLA certainly had no problem being in Wuhan in October, once the Games were over and the pandemic kicked into gear, they stayed clear. And besides, we now know that the wet market wasn’t the initial source of the virus anyways, however it turns out that a map of Wuhan’s general commercial density:
…Provides almost an identical overlay to the incidences of initial cases, which is exactly what would be expected if an oral live-attenuated vaccine had begun to reemerge from the military personnel gathered for the Wuhan Military Games and spread to the over 250,000 others who were brought in to help make the Games happen.
The first case ever identified were in fact in a PLA military hospital, as were most of the earliest clusters of cases, and this first case seems to clearly be an ancestor of the strain found at the wet market. And perhaps most tellingly, all of the earliest cases show up only in hospitals serviced by just one metro line, the same one which services the WIV.[i]
So the largely asymptomatic spread of a deattenuating live-attenuated vaccine only just beginning to become airborne would explain the fractal and unexpected nature of new pockets of infection, as well as what’s been described as EVALI in America. This odd medical puzzle could have been stray swarms of the novel coronavirus that made their way to the West, but too weak once they got here to create more than passing symptoms before fluttering out - so EVALI was simply quasispecies swarms only managing to flitter lightly across the populations they encountered before burning out.
On the other end of that spectrum was the solution that the PLA likely attempted on the citizens of Wuhan once they realized the virus was airborne and deattenuating out of control, a solution which created the need for draconian lockdowns and gave videos of people collapsing in the street to the world: Discovering a novel airborne RNA virus, the CCP applied some of the lessons learned attempting to vaccinate against another airborne coronavirus, Feline Infection Peritonitis Virus (FIPV), and attempted design a bespoke live-attenuated vaccine with a select groups of genes removed in an attempt to retard its swarm’s overall virulence.
This approach has been on the table for decades, since it was seen to possibly “allow the development of vaccines against infections with other pathogenic coronaviruses, including that causing severe acute respiratory syndrome in humans.”[i] And although it can be incredibly effective if the right genes are removed, take away the wrong ones and 80% of your subjects drop dead inside a month.
And so desperately attempting to contain the growing pandemic, the CCP rushed out a gene-removed live-attenuated vaccine - applying it not to its retreated military already outside the city limits, but instead only to the hapless citizens of Wuhan. Creating a mass casualty event as the bespoke vaccine burned too hot, effectively stopping the swarm but only by killing off its hosts and creating so much death that the Chinese government began welding apartment buildings shut, unsure if this newly juiced swarm would be able to escape the city or only consume the hosts it was administered to.
The awareness that the COVID-19 Pandemic was caused by an orally-administered live-attenuated virus which needed to be able to form robust quasispecies swarms to deattenuate would also explain China’s insistence around the viability of a “cold chain” hypothesis involving frozen food, since at some point it will likely become apparent that early strains of SARS-CoV-2 have an odd preference for our intestinal tract. Originally being an orally-administered LAV also fits how well-acclimated the novel coronavirus already is to the cold, since it needed to change just one-tenth of one-percent of its amino-acids as it was acclimated from 37-degrees C to 22-degrees C in cell culture.
And an orally-administered live-attenuated virus and quasispecies mutant swarm beginning to deattenuate far faster than it was supposed to and overheat its hosts with infections would also explain the CCP’s insistence on collecting anal swabs. This method seems to be the only way to accurately detect asymptomatic infections from discharged hospital patients, which is likely related to the fact fecal samples reveal much more about the composition of the quasispecies mutant swarm: Yielding more inactive virus, capturing far more genetic distance, and showing a much wider range of mutations.
And so the CCP’s insistence on anally swabbing absolutely everyone, and especially kids, is almost certainly due to the fact that this is the only way to accurately track the shape of the quasispecies mutant swarm, and prevent it from deattenuating enough to become even more virulent than it already has in much of the world.
However it’s not just all of this logistical and technical evidence that supports to SARS-CoV-2 being a once-attenuated SARS-like LAV making its way back towards its original V-1000 form, an enormous amount of molecular evidence leans that way as well.
11.3 – If it quacks like an orally-administered live-attenuated vaccine…
As it’s recently been pointed out, the WIV has been working on pan-coronavirus fusion inhibitors which they claim works on five different human coronaviruses including the original SARS-CoV and MERS-CoV, as well as three additional SARS-live bat-borne coronaviruses.[iv] All this would be hard to do without a pan-coronavirus, or at least the plans to create one in the first place.
Researchers found that after comparing the products of nearly 200 proteins across seven human coronaviruses, that “the genes encoded by SARS-CoV-2 are generally more potent immune suppressors than their homologues from the other coronaviruses,” including the temporally paradoxical observation that “SARS-CoV-2 proteins are more potent in their inhibition of innate immune signaling than the corresponding SARS-CoV-1 protein.”
There’s also a novel gene named CaORF15, which encodes a protein which has never been seen before other than in RaTG13,[v] which is a consensus sequence with no natural providence either, and was likely a less-attenuated version of SARS-CoV-2 anyways.
This protein appears to interfere with the process of interferon accumulating which is necessary for a full immune response by using the STING pathway, a fundamental part of our immune defense system meant to neutralize DNA-based pathogens and tumors, and sticks out on a purportedly bat-borne RNA-virus like a unicorn-horn growing out of the anus of a hairless cat. However, this is the kind of activity that has been directly sought in vaccine design,[vi] and strangely it appears as though this gene was somehow under “a pressure to evolve CaORF15 and then to maintain it” [vii] within a population of bats.
As the authors note: “The presence of CaORF15 within the Spike coding sequences means that nucleic acid-based vaccines based on the natural Spike coding sequence – depending on their design -could also encode the CaORF15 protein, which may be immunosuppressive in a vaccine context. However, Pfizer’s vaccine is based on a codon-optimized version of Spike in which the AUG of CaORF15 is changed to ACG.”[viii] Don’t worry, nothing to see here, just some bats with extremely advanced degrees.
And in a different region of the genome called ORF6, the proteins “produced more efficient antagonists of innate immunity than their orthologs from SARS-CoV lineages,”[ix] another effect that you’d want from a live-attenuated vaccine, but wouldn’t be expected to evolve in nature unless a bat colony was planning on putting on a production of Rent.
Since its emergence one of SARS-CoV-2’s most notable aspects was what appeared to be the incredibly high-fidelity of its proofreading enzyme, especially notable since “controlling replication fidelity is a promising approach for engineering live, attenuated vaccines,” and observation that was made after high-fidelity variants were found to provide superior protection and less drug resistance when used against a barnyard RNA virus named Foot-and-Mouth Diseases (FMDV). [x] And not only does its proofreading enzyme indicate a vaccine-related origin, lots of other molecular clues do as well.
The first draft of Sirotkin & Sirotkin’s look at a possible lab origin noted SARS-CoV-2’s extreme CpG dinucleotide deficiency and noted that ferrets in addition to canines seemed amenable to the rate it was found in the novel coronavirus,[xi] another tell-tale sign of involvement with the vaccine development which so often used serial passage.
And this ratio also provides an answer to the unnatural relationship between SARS-CoV-2 and RaTG13, since the CCP may have sent the military into the WIV a few days after RaTG13’s genome was submitted for publication since it provides an excellent possible template for SARS-CoV-2 being codon-usage deoptimized from it, another approach used in the development of live-attenuated viruses although thought to make them more stable.[xii]
Specifically, the efficacy of increasing the CpG dinucleotide deficiency of the poliovirus strain used for a vaccine across not even 10% of its genome led to the conclusion that: “Replacement of natural codons with synonymous codons with increased frequencies of CpG and UpA dinucleotides may offer a general approach to the development of attenuated vaccines with well-defined antigenicities and very high genetic stabilities.”[xiii]
And since every sin leaves its mark, the fundamentally unnatural origins of SARS-CoV-2 is revealed even further by the fact it is able to trigger the Original Antigenic Sin from one family of virus while having its origins clearly in an entirely separate one. This is an evolutionary non sequitur, since after one study demonstrated that sustained COVID-19 infections that overtime more protection was produced against HCoV-OC43’s spike that its own, in an apparent expression of Original Antigenic Sin,[xiv] that should’ve defined SARS-CoV-2’s infective family and provided clues to its origins – not a paradox.
Paradoxical because HCoV-OC43 is a coronavirus that’s been endemic to humans for at least 100 years, possibly originally jumping into humans during a bovine-based pandemic in the late 19th century, and traces its origins through cows and back to mice.[xv] No bats to be found.
The only thing that could leave this kind of mark, to violate the laws of Original Antigenic Sin this way as it scythes through human lives by the thousands… well, it’s certainly not natural.
And in one final genome-defying trick, as it spreads across the populations of three entirely different species, it is seeking the same epistatic-gatekeeping mutations in all of them: Humans, mink, and lab mice are all displaying the same epistatic mutations simultaneously and across continents.[xvi]
That’s the sign of gatekeeping and a vaccine-derived-virus working its way back to full virulence, not natural evolutionary behavior.
11.4 – “We modified our science team to remove ethical restraints.”
Shortly after our peer reviewed paper was published in BioEssays, what seemed like a benign group of scientists reached out to me and my dad about our claim the 1977 H1N1 leak had in fact been subject to gain-of-function research. We immediately replied with the link that’d gotten accidently elided as we explained in our addendum, and then that was it.
At the time, I assumed one of the group was some old contact or another of my dad’s, since it wasn’t like this was his first rodeo, although it had been awhile, and figured it was just a friendly query. But then it would turn out that one of them, Gigi Kwok-Gronvall, would turn up a few weeks later coauthoring John Hopkins papers which dismissed my father’s career as irrelevant to the task at hand, and which waved their hands at our peer reviewed paper without making one single critique at all.
This pattern of refusing to give a single solitary critique while acting as if our paper shouldn’t have passed peer review and get published was continued a few weeks later, after Boston Magazine published an article that’ll be used in English classes for the rest of human history as an example of modern corporate propaganda.
Ignoring the international global news splash Zero Hedge had made getting kicked off Twitter for alleging a laboratory origin, and the fact that BioEssays had already published an explanation of how laboratory engineering may well have been involved that had one of his generation’s most experienced bioinformaticians as lead author – this article was likely commissioned right around when Gigi Kwok-Gronvall and her fellow DARPA-linked friends were trying to pick holes in our peer reviewed paper, based on the timing of it all.
And tellingly, the article pushed a post-doc with a pre-print as someone who should be the go-to science contact for a possibly laboratory origin, instead of the actual scientists being peer reviewed and published about it. And that post-doc is someone representing the same Broad Institute whose cofounder is currently organizing a call for Dr. Charles Lieber’s release, and who also refuses to engage with our paper at all – seeming to allege there’s something improper about its publication.
Charles Lieber is a man who’s alleged to secretly have accepted blood-money from a regime which regularly gang-rapes members of an ethnic and religious minority in concentration camps. This is someone who Stuart Schreiber, who’s used to bending the scientific community to his will, and co-founder of the MIT and Harvard’s Broad Institute, thinks should be treated more kindly by the Department of Justice, to make sure that there isn’t a “chilling effect” on international collaboration.[xvii]
This is the same Broad Institute which has been sending out one of its representatives to run interference against legitimate academic inquiry and the scientific process, to protect the vested interests of multi-billion dollar corporations, and telling journalists to ignore peer review and the scientific publication process.
Maybe Schreiber wants more of the international collaboration that’ll lead to cutting-edge chimeric viral engineering like Dr. Baric was doing at UNC ending-up back in at the WIV and eventually the PLA? So to make sure there’s more of that, he wants closer ties to a regime which forces children to slave in cotton farms and men to watch as their wives and daughters are raped in front of them?[xviii]
Prison taught me a whole bunch, and one of the things I realized along the way is that just like in pretty much every penal facility, I was surrounded by far more sociopaths than I would be in the general public. Studies have consistently estimated prisons to hold roughly 10-20% sociopaths, with the general population only having about 1%.
But it wasn’t the first time I noticed being surrounded by an unusually high concentration of sociopaths, since if my four years at Harvard taught me anything, it was that sociopathy also tends to concentrate among the ultra-wealthy the same way it does the most desperately poor.
Perhaps that helps explain the recent approach modern medicine has taken, which is very obviously about maximizing profits far before public health. As Goldman Sachs has already openly presented the investor reality that there’s no money to be made from actually curing people with revolutionary and ground-breaking science, pointing-out that a one-shot gene-therapy treatment didn’t need to be repeated and so might have an issue with “cash flow.”[xix]
So almost like renting out software instead of selling it, forcing everyone to constantly pay for upgrades and be unable to outright purchase anything – because wow would that be just blatantly unethical and greedy – now pharmaceutical companies are planning on selling a never-ending chain of vaccines for a pandemic their research almost certainly helped seed, instead of addressing the underlying general public health issues ranging from better ventilation to nutritional deficiencies, which can help protect everyone from all quasispecies swarms.
Because of course the most lucrative cinematic franchise of all time didn’t just introduce the idea of the military-industrial complex rolling in to save the entire world from a monster which threatens to consume all of humanity in its fiery embrace, one that’s actually entirely of their own making, using their own charismatic but clearly ethically compromised and self-promoting “hero” to do it?
Since if its one thing the military-industrial complex hates its getting their toys taken away, since if they technology is already out there shouldn’t they be able to use it before the Bad Guys get their hands on it?!
America and the rest of the world likely doesn’t have too much longer to navel gaze at this thing and ponder how a “natural” virus could have such unusual behavior and continually surprise the “experts” who’ve been demonstrably wrong over and over again since the first months of this pandemic.
And Brazil’s new virulent P.1 variant is estimated to be mutating sixteen-times faster than any strain before it, a rate whose increase may be only starting to accelerate, as there’s no way to know for sure exactly what the V-1000 its attempting to get back to looked like or how much longer it has to go.
However the prospect that the COVID-19 Pandemic actually represents a global version of an oral live-attenuated virus transmitting widely enough to deattenuate back to its original fully-virulent V-1000 form should be more than enough to spur public health authorities into action with basic guidelines around simple mechanical barriers like masks and extra ventilation, which done in piecemeal and often alone seem to have been enough to keep the seasonal flu’s quasispecies swarm from forming at all this past year.
History isn’t written yet, but with billionaires’ getting 54% richer just during the pandemic, it’s hard to imagine a world that doesn’t have their grip on it – shaping the reality you perceive. But luckily for us, humanity has been defined by getting out of exactly this sort of situation, and it turns out that all the clues we needed to find the origins of our most recent common ancestor and our very humanity, were right there in the Truman Show all along.
Come back in a few weeks to find out how in a few weeks!
Epilogue.
In one of those strange twists of fate, many years after desperately trying to run me down and plea for help from within the cruel confines of Ft. Detrick’s BSL-4 Research Labs, and after having spent my own time behind those wires, I would reunite with that poor downtrodden lab-monkey - who’d sadly been turned into a sociopathic gaslighting sockpuppet - and begin what would go on to become D.R.A.S.T.I.C.
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Special Thanks: Some dude who bangs my Mom, Anonymouse, and the Silver Fox.
Substack ate my citations, the entire article is available as a PDF on Dropbox here.
[i] Haijema, Bert Jan, et al. “Live, Attenuated Coronavirus Vaccines through the Directed Deletion of Group-Specific Genes Provide Protection against Feline Infectious Peritonitis.” Journal of Virology, American Society for Microbiology Journals, 15 Apr. 2004, jvi.asm.org/content/78/8/3863.
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[i]https://edis.ifas.ufl.edu/ps032#:~:text=Pathogenic%20avian%20influenza%20was%20first,It%20was%20eradicated%20both%20times.&text=In%201996%E2%80%931997%2C%20a%20number,positive%20for%20H7N2%20avian%20influenza. [ii] Gompo TR;Shah BR;Karki S;Koirala P;Maharjan M;Bhatt DD; “Risk Factors Associated with Avian Influenza Subtype H9 Outbreaks in Poultry Farms in Kathmandu Valley, Nepal.” PloS One, U.S. National Library of Medicine, 2006, pubmed.ncbi.nlm.nih.gov/32240166/. [iii] Gompo TR;Shah BR;Karki S;Koirala P;Maharjan M;Bhatt DD; “Risk Factors Associated with Avian Influenza Subtype H9 Outbreaks in Poultry Farms in Kathmandu Valley, Nepal.” PloS One, U.S. National Library of Medicine, 2006, pubmed.ncbi.nlm.nih.gov/32240166/. [iv] Gompo TR;Shah BR;Karki S;Koirala P;Maharjan M;Bhatt DD; “Risk Factors Associated with Avian Influenza Subtype H9 Outbreaks in Poultry Farms in Kathmandu Valley, Nepal.” PloS One, U.S. National Library of Medicine, 2006, pubmed.ncbi.nlm.nih.gov/32240166/. [v]http://www.fao.org/poultry-production-products/production/en/[vi]https://jvi.asm.org/content/93/1/e01740-18[vii]https://pubmed.ncbi.nlm.nih.gov/23577628/[viii]https://jvi.asm.org/content/93/1/e01740-18[ix]https://jvi.asm.org/content/93/1/e01740-18[x]https://jvi.asm.org/content/93/1/e01740-18[xi]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7435492/[xii] The author would like to notify the AP Board that several of the tests in his general vicinity may have been somewhat loosely cribbed off of his; congratulate Mr. Hartswick, whose first name he really doesn’t remember, for inspiring the character Walter White and for his patience and dedication, and to express the hope that he gets to share a beer with Richard Wrangham someday. And finally apologize to everyone he hit in the face with turtle testicles during lab. Sorry about that, I was aiming for your mouth.
[i] Ratto-Kim, Silvia, et al. “The US Military Commitment to Vaccine Development: A Century of Successes and Challenges.” Frontiers, Frontiers, 5 June 2018, www.frontiersin.org/articles/10.3389/fimmu.2018.01397/full#B10. [ii]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3317607/[iii]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3317607/[iv]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3317607/[v] Ratto-Kim, Silvia, et al. “The US Military Commitment to Vaccine Development: A Century of Successes and Challenges.” Frontiers, Frontiers, 5 June 2018, www.frontiersin.org/articles/10.3389/fimmu.2018.01397/full#B10. [vi] Oxford, John S., and Douglas Gill. “A Possible European Origin of the Spanish Influenza and the First Attempts to Reduce Mortality to Combat Superinfecting Bacteria: an Opinion from a Virologist and a Military Historian.” Taylor & Francis Online, May 2019, www.tandfonline.com/doi/full/10.1080/21645515.2019.1607711. [vii] Oxford, John S., and Douglas Gill. “A Possible European Origin of the Spanish Influenza and the First Attempts to Reduce Mortality to Combat Superinfecting Bacteria: an Opinion from a Virologist and a Military Historian.” Taylor & Francis Online, May 2019, www.tandfonline.com/doi/full/10.1080/21645515.2019.1607711. [viii] Adalja, Amesh A, and D A Henderson. “Original Antigenic Sin and Pandemic (H1N1) 2009.” Emerging Infectious Diseases, Centers for Disease Control and Prevention, June 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC3086248/. [ix] Reid, Ann H., et al. “Origin and Evolution of the 1918 ‘Spanish’ Influenza Virus Hemagglutinin Gene.” PNAS, National Academy of Sciences, 16 Feb. 1999, www.pnas.org/content/96/4/1651.
[i] https://onlinelibrary.wiley.com/doi/10.1002/bies.202100017 [ii] Ratto-Kim, Silvia, et al. “The US Military Commitment to Vaccine Development: A Century of Successes and Challenges.” Frontiers, Frontiers, 5 June 2018, www.frontiersin.org/articles/10.3389/fimmu.2018.01397/full#B10. [iii]https://www.statnews.com/2018/09/03/flumist-vaccine-recommendations/[iv]https://www.statnews.com/2016/06/22/flu-vaccine-mist-children/[v]https://www.eurekalert.org/pub_releases/2021-03/uocm-hvd031721.php
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