The Lab Origin of SARS-CoV-2 By Chris Knight (Florida)

I have not seen much recent material on the lab origin of SARS-CoV-2, our beloved Covid-19, the interest has gone a bit cold with on-going tyranny taking centre stage. Still, here is interesting material, somewhat technical, discussing the significance of the furin-cleavage sites on the Covid virus. Influenza viruses do not normally have this, it is said, so something odd must have gone on, via gain-of-function engineering.

https://harvard2thebighouse.substack.com/p/a-grin-without-a-cat

“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.

Although it started as a point of obscure technical reference back in early 2020 as our ongoing pandemic was still in the early stages of spreading its now-ubiquitous wings, it’s now nearly two years later and debates are still raging about the origins and relevance of SARS-CoV-2’s notorious furin-cleavage site, or FCS. 

This four-base amino-acid insert immediately drew the attention of the Sirotkin & Sirotkin father-and-son team as they were working on their paper covering the possible laboratory-engineered origins of the COVID-19 Pandemic, which was submitted back in April 2020, long before anyone else was discussing any of this with meaningful scientific detail:

The genetic signatures in question includes two distinctive features possessed by SARS-CoV-2's spike-protein: the unique sequence in the receptor binding domain (RBD), a region known to be critical for SARS-CoV-2's utilization of human angiotensin converting enzyme (ACE2), which is the cell surface receptor used by both SARS-CoV and SARS-CoV-2 for fusion with target cells and subsequent cell entry. The second feature is the presence of a polybasic furin cleavage site, which is also known as a multibasic cleavage site (MBS)—a four amino acid insertion with limited sequence flexibility—within the coronavirus's novel spike-protein, that is not found in SARS-CoV or other lineage B coronaviruses. 

This furin cleavage site, which is poly or multibasic by definition since its composed of multiple basic amino acids, is an important virulence feature observed to have been acquired by fusion proteins of avian influenza viruses and Newcastle Disease Virus either grown under experimental conditions or isolated from commercial animal farms—settings that mimic the conditions of serial laboratory passage. 

In fact, no influenza virus with a furin cleavage site has ever been found [to originate] in nature, and it is a feature that has been thoroughly investigated in the literature since it appears to allow the influenza viruses that carry it to establish a systemic multiorgan infection using different cell types including nerve cells,  is correlated with high pathogenicity, and also plays a key role in overcoming the species barrier.  

More generally, despite the fact that not all serially passed viruses have demonstrated an increase in pathogenicity, the fact remains that every highly pathogenic avian influenza virus, defined by having a furin cleavage site, has either been found on commercial poultry farms that create the pseudo-natural conditions necessary for serial passage, or created in laboratories with gain-of-function serial passage experiments.

The first glaring sign that the virological community had something to hide was the fact that all of the studies covering the notorious 2012 gain-of-function experiments with ferrets and influenza referred to this four amino-acid FCS insert as multi-basic instead of poly-basic, like it was in all of the 2020 studies discussing this feature in the SARS-CoV-2 virus. 

Granted scientific writing always has a load of jargon, but this really seemed intentional, to try a little syntactical shield to draw attention away from the serial passage gain-of-function experiments down with ferrets back in 2012 by hiding behind the fact that polybasic was somehow different from multibasic. 

However there’s still something that seems to get in the way of tying SARS-CoV-2’s FCS directly to serial passage gain-of-function vaccine work, since there doesn’t appear to be any molecular room for SARS-CoV-2 to have gotten its FCS simply during serial passage as an insert, as it apparently occurs with influenza viruses during serial passage. Based on the genetics involved, there doesn’t appear to be any clear genomic pathway for SARS-CoV-2 to have gained it’s four amino-acid FCS insert as influenza strains presumably did back in 2012, allowing our novel coronavirus to molecularly spread its wings and achieve airborne transmission. With influenza the insertion matches up based on what we know about assumed genomic behavior, with our novel coronavirus that isn’t the case.

So which is it, does the FCS lead us conclusively to a laboratory origin or not? 

“You may have noticed, I’m not all there myself.”                                                                 

- The Cheshire Cat

In 2012 during the serial passage experiments with ferrets and influenza viruses, two different teams carried out similar experiments with the H5N1 strain of influenza, which was and still is proliferating all across large commercial poultry farms, and back then was beginning to draw concern that it might gain the ability to jump all the way into human populations - isolated cases had emerged in farm workers in close contact with poultry all across the globe in the years leading up to these gain-of-function experiments, but there way no recorded human-to-human transmission yet. 

It’s probably worth a brief moment to consider that every major industrial poultry farm on earth is stuffed to the wattles with potential viral hosts which are unable to self-segregate when they get sick like they are in wild populations, and so despite the fact that modern poultry farms have vaccination programs with 100% genomic coverage, 100% compliance, and 100% surveillance  - a perfect experimental situation with far more controllability that human societies - the emergence highly-pathogenic influenza strains that easily cull half the flock in a matter of days and sometimes result in 100% mortality are a constant threat. 

Turns out you can’t vaccinate your way out of highly-transmissible RNA viruses in crowded commercial settings, but it also turns out that humans have a little issue trying to play God, and as so here we are. 

So the H5N1 strain being used for serial passage experiments back in 2012 was a close cousin to the H1N1 1918 pandemic strain: Instead of spike-proteins like coronaviruses, the part of an influenza virus that is able to access host receptor-cells consists of a hemagglutinin protein right next to a neuraminidase protein, both of which come in different assortments, and so are referred to together as HxNy - with numbers from 1 to 18 possible to represent the different hemagglutinin proteins, and 1 to 11 indicating which neuraminidase protein is present.

So as a unit, the HxNx surface-protein complex in influenza viruses fills an analogous role - penetrating and successfully infecting host cells - as the spike-protein does for coronaviruses, where SARS-CoV-2 has its FCS. 

In the first experiment with H5N1, a Japanese team lead by Dr. Yoshiro Kawaoka wanted to try and measure how likely this strain was to move past only jumping from poultry to people and actually establish human-to-human transmission, by taking the gene for the H5 protein from H5N1, and splicing it onto a virus with the seven other genes - not including this H5 hemagglutinin gene - from the pandemic H1N1 strain, and then seeing what happened when the strains that emerged from this process got a chance to infect a bunch of lab ferrets sharing air in the same room but isolated in separate cages. 

A Dutch team lead by Dr. Ron Fouchier conducted a similar study, in this one they also took this H5N1 influenza strain, but instead of making a chimeric Frankenvirus with genes from H1N1, alternatively but to a similar effect: they jacked it full of mutagens to accelerate the evolutionary process, and then also let it run amok through a whole bunch of lab ferrets in a similar set-up - watching to see which strains were eventually able to establish airborne transmission among the critters. 

And in both cases it was only strains with our notorious FCS, albeit described without that exact term and instead using multibasic inserts and other language, which were able to reliably establish airborne transmission between laboratory ferrets, telling both teams of scientists it was this furin-cleavage site which was especially dangerous and might open the door to another human influenza pandemic if a virus with it was able to jump completely off of poultry farms and into human populations. 

However there’s been a fundamental misunderstanding going on, one that rests at the very base of scientific exploration, that’s caused everyone talking about the FCS to argue that it’s an insert that appeared within the virus during these serial passages between ferrets, and was an evolutionary adaptation which allowed for airborne transmission to occur. 

Because if you look carefully, that’s not what happened at all. 

“How queer everything is to-day! And yesterday things went on just as usual, I wonder if I’ve been changed in the night? Let me think: was I the same when I got up this morning?”

                       -The Cheshire Cat

Fortuitously for us, the easiest way to correct the misconception around the FCS only emerging after airborne transmission between animal hosts, or being an insert that got added directly into the genome by evolution as a response to that pressure, is to examine SARS-CoV-2 and its behavior during serial passage as a quasispecies mutant swarm.

The quasispecies swarm model approaches RNA viruses not as discrete genotypes transmitted on by discrete strains, but instead as quasispecies of mutant swarms of virions which carry distinct but complimentary sets of alleles - collections of genes thought to work together - which work in concert in real-time to establish and expand infections. One of the first empirical changes that comes once you consider an RNA virus as a quasispecies is that at any point in time an average of all the extant variants’ genomes serves as the smallest selective unit, as opposed to using individual virions or any single extant genome in a population, the classical approach. 

This quasispecies viral swarming is an amorphous behavior that describes the search for fitness that occurs as each successive generation of the swarm produces another spectra of mutations, with the term “quasispecies” specifically describing “distributions of non-identical but related genomes subjected to a continuous process of genetic variation, competition, and selection, and which act as a unit of selection.”

Each of these distributions can be considered clouds of allelic statistical possibilities, each of which represents the spectrum of mutations that can be expected to emerge within a set number of generations, so their ratios will be constantly changing over successive generations and in different environmental settings.

This type of effect has just begun to be explored within the classical model, by quantifying the antigenic waves that shimmer across the surface of quasispecies mutant swarms as they shift between the host populations, and using these measurements to indirectly measure the quasispecies swarm itself without really getting the full picture of what’s really going on. 

With quasispecies viruses replicating continually once a successful infection has set in and begun to smoulder, the most-fit variant for a given tissue will predominate in that one tissue when a sample is taken only from it. However, although only one variant will appear in the smoky quasispecies mutant swarm infecting the tissue, the smouldering infection will be continually throwing off new variants which represent different points in the possible mutational spectrum – some of which will be better adapted to neighboring tissue, and others acting as accelerants for the predominate variant, intensifying its virulence.

And just like one gas acting as an accelerant for another’s combustion can be modeled mathematically by looking at their relative binding tendencies to different elements and how they react at different concentrations, the mathematical inevitability of quasispecies mutant swarms fully exploring their mutational spectrum and finding variants to fuel their spread isn’t any different. It’s only the language that varies, as the literature currently describes the positive selection quasispecies mutant variants resulting in “hitchhiking” between mutations on variants in the same swarm, the exact same concept as different variants and their mutations acting as accelerates for each other during gaseous chemical combustion.

Or in a more traditional sense, quasispecies mutant swarms likely depend on a sort of accidentally eusocial viral altruism to prosper. As one study revealed, although its usually possible to identify a majority consensus sequence from a sample of a host infected by COVID-19, the sample had a broad median variant count of 23, with nearly 250 different variants found in total just within one single host. 

And considering that about half of the observed mutations thought to have a significant impact on gene expression and samples differing throughout the day even in the same organ system, as well as the fact that barely 2% of the minority variants were found to overlap at all between any two hosts - the inherently nebulous quasispecies mutant swarming nature of SARS-CoV-2 begins to coalesce even more.

So as with any virus, but especially with coronaviruses, it’s important to keep in mind that hidden within their large genomes are entire suites of accessory genes which only appear functional while actually living inside their hosts, in vivo, and whose function won’t be observable within the virtual environment in lab Petri dishes, in vitro: “the coronavirus group-specific genes are not essential for growth in cell culture but function in virus-host interactions.”

This means that some coronavirus genes get effectively muted when the virus isn’t being challenged by the immune system of an entire host body, which also helps explain why SARS-CoV-2 violates the “canyon hypothesis,” and has a region of its genome which appears never to have been challenged by a full host immune system like every other human coronavirus. 

And so with the quasispecies model in mind, maybe it shouldn’t be such a surprise that our friendly neighborhood novel coronavirus has an FCS that isn’t exactly permanent, and can pull a little bit of a disappearing act - or at least what appears to us as outside scientific observers to be a disappearing act. Since it turns out SARS-C0V-2’s quasispecies swarm almost immediately loses its FCS when it’s passaged through Vero cells, which are derived from a line of African green monkey kidney cells that’s commonly used for cell culture, or in vitro, experiments.  

These cells don’t present the same set of immune challenges as a full host, hardly a tiny fraction of them, and so it turns out SARS-CoV-2’s quasispecies swarm no longer needs the group-specific genes to cleave certain cell types conferred by an FCS when it’s in these friendly isolated cell-culture kidney cells - meaning it drops off, almost entirely in a single passage. 

Almost, but not entirely. A phrase that defines trying to understand quasispecies mutant swarms overall. 

But okay, the FCS can be almost entirely lost without all the immune challenges posed by a full host, but then how did it get there in the first place? The exact same way the H5N1 strains “gained” it during the 2012 experiments with ferrets and influenza: It was always there to begin with. 

“When the day becomes the night and the sky becomes the sea, when the clock strikes heavy and there’s no time for tea; and in our darkest hour, before my final rhyme, she will come back home to Wonderland and turn back the hands of time.”

                             - The Cheshire Cat

In each of the 2012 serial passage experiments with influenza strains and ferrets, the FCS didn’t appear as a response to the challenge of airborne transmission between hosts, it existed in a very small frequency within each H5N1 swarm prior to each experiment, and then quickly reached majority status once the bottleneck of jumping from ferret-to-ferret in the air was presented. 

It was observed by each team after successful airborne transmission between ferrets, however before this challenge was presented to the H5N1 swarms, they were both first heavily mutated by artificial outside means - directly splicing in genes from H1N1 in the case of Dr. Yoshiro Kawaoka and bathing the swarm in a mutagen in the cast of Dr. Ron Fouchier - artificial, inherently sloppy, and unpredictable processes a long way from surgically splicing precise nucleotides in-and-out, which led to the emergence of the FCS in small minority subpopulations of their swarms prior to their presentation to ferrets for passaging.

This was the challenge that created the FCS during those experiments, the outside intervention of scientists intent on carrying out their gain-of-function experiments, not the challenge of jumping through the air between ferrets. Once it exists anywhere in the swarm, the FCS is going to remain at levels that are too small for typical detection until its special ability is called for: Airborne transmission between mammalian hosts. 

Directly supporting this is the reemergence of SARS-CoV-2’s FCS within Calu-3 cells - cells grown from the surface of human lungs - after it falls off in Vero cells. The swarm doesn’t need an FCS to flourish inside monkey kidney cells, inside Vero cells, however once it gets placed into human airway cells - now the chance of airborne transmission is back on the table, and so the FCS quickly returns to dominance inside the swarm, reaching fixation in just a single passage. 

SARS-CoV-2’s affinity for human kidneys - up to 25% of its patients can suffer an acute kidney injury - is likely linked to this past history being passaged through Vero kidney cells during its development as a live-attenuated vaccine (LAV) - a vaccine built from an entire virus that’s supposed to be weakened down to the point where it can never establish symptomatic infections, but still serves as enough of a mock-up to provide our immune systems with the ability to recognize and neutralize the actual live version of that virus. 

LAVs were discovered by Louis Pasteur of preserving dairy-products fame, who accidentally discovered that samples of chicken cholera left out in the elements got weakened to the point where they effectively became vaccines: Exposing healthy chickens to samples of cholera that’d been weakened, or attenuated by the elements, protected the chickens from infection by the full-strength virus without creating any symptoms during inoculation by the weakened strain. And although this version of a LAV wasn’t known to revert, the modern LAV that protects against Polio, called OPV, can and does revert all the way back to full virulence and cause paralysis in its hosts. 

And to design a LAV against Yellow Fever, the only type of vaccine that would confer protection since it creates the strongest type, the first step was building a highly-pathogenic chimera built from genes of several different strains of that virus. This was also the first step to develop OPV, which has recently begun the paradoxical phenomenon of reassembling itself within vaccinated populations and establishing full paralytic virulence. In 2019 there were 176 cases of poliomyelitis derived from the OPV strain reverting back to virulence worldwide, when only 33 had been seen the year prior. 

This enigmatic process, of a LAV reverting or deattenuating back to virulence, is one of the worst nightmares for the virological and vaccinological communities - in part because in the case of OPV, the fully reverted strains are able to infect absolutely everyone, even if they’ve been fully vaccinated or previously infected. And it’s a possibility virologists and vaccine-designers are all well-aware of.  

After all, as our Dr. Ron Fouchier of ferret and influenza serial passage gain-of-function fame noted rather presciently in July of 2019, a few months before the start of the Wuhan Military Games:

“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 when a LAV reverts, the viral swarm that emerges in the case of OPV at least runs right through both natural and vaccine-induced immunity, and this is even with a virus like Polio where the OPV vaccine is considered 100% effective and permanent. 

Turns out OPV vaccine was almost, but not entirely effective. 

And so SARS-CoV-2 and the experimental H5N1 viral swarms both expressing their FCS when they need to achieve airborne transmission serves as a canonical example of  “the convergent evolution that dominates virus–host interactions, since viral proteins evolve convergently and often accumulate many of the same linear motifs that mediate many functionally diverse biophysical interactions in order to manipulate complex host processes.” They’re both products of serial passage gain-of-function experiments, and both display the ability to gain and lose their FCS depending on whether or not mammalian airborne transmission is on the table.

When SARS-CoV-2 is taken out of kidney cells where an FCS won’t possibly be needed for airborne transmission, it seems to disappear back into the shadows as it only remains within a small minority sub-population of the swarm, but when it’s placed back in human airway cells - in just one passage it can appear to reach fixation, although in reality there will always be a small minority subpopulation without it.

But of course in the case of SARS-CoV-2, this ability for the minority population with the FCS to almost immediately become the dominant strain wasn’t first observed in the laboratory, but unfortunately for humanity occurred in the field during the Wuhan Military Games, when this unexpected emergence of the FCS-dominant swarm allowed for airborne transmission and kicked off our pandemic as the virus spread through the air all across Wuhan.

The fact SARS-CoV-2 had an FCS in the first place was suppressed from the start, because of its obvious ties to the gain-of-function serial passage work of 2012. And because of the nature of quasispecies swarms, which often create the illusion that only one discrete variant is extant in a population since each isolated organ system tends to predominately host the variant that’s best suited for it at the time, this novel coronavirus appeared to have a rather immutable and stable genome - since nasal swabs will only ever catch the one variant happens to be winning in your nose at a given time. 

However the full quasispecies swarm will always be there, it’s just not going to appear unless you look for it with far more exacting tools than just a nasal swab. And just like OPV and its perpetually reverting quasispecies swarm, SARS-CoV-2 is going to continue to revert back towards its original highly-pathogenic form so long as any transmissions are ongoing at all, going through gatekeeping mutations as it makes unexpected evolutionary leaps back towards full virulence. 

“Only a few find the way, some don’t recognize it when they do – some… don’t ever want to.”

                              -The Cheshire Cat

H1N1 is the highly-pathogenic state of human influenza, it is not an alien virus - it is completely and entirely adapted to our genome and has been with us for thousands of years. H1N1 doesn’t create a pandemic by simply by existing in a population, it is the strain that wins out and emerges once there’s enough crowding and transmission events to trick human influenza into thinking that its host population is about to die off completely, and so it goes into a highly-pathogenic state in an attempt to jump into a new host species, in its case from humans and into pigs.  

Highly-pathogenic avian influenzas are identified by the existence of an FCS, something H1N1 doesn’t need for our cells because its perfectly adapted to human populations to begin with: 

“In 1997, small fragments of viral RNA were obtained for sequence analysis from an autopsy sample of a victim of the 1918 influenza. The initial characterization of the virus confirmed the H1N1 subtype and demonstrated that the 1918 HA did not possess the cleavage site mutation seen in the lethal H5 and H7 viruses. This finding eliminated the HA cleavage site mutation as an appealing explanation for the virulent behavior of the 1918 virus.”

And although there haven’t been any more published gain-of-function experiments with avian influenza due to the very-selectively-enforced moratorium against the practice, in the years since poultry farms have served as their own handy real-life Petri dishes. 

Studies of the H7N9 avian influenza as its emerged off of poultry farms in a highly-pathogenic state and managed to infect workers have revealed that the process of jumping from birds into people doesn’t just happen out of nowhere in one magic moment. In fact, it takes five successive waves of infections before the H7N9 swarm begins to regularly jump from birds into farm-workers, the only people in close-enough contact to the avian swarm for all five of these waves to antigenically wash over them, building up a swarm within their prospective new humans hosts, and also slowly altering the nature of H7N9’s swarm within both host species. 

And of course since there’s a highly-pathogenic avian influenza forming, the FCS is the distinguishing feature found in the fifth wave that indicates humans are now at risk. However it’s not only found in the fifth wave, and begins to show up in earlier waves along with other genomic features that fully reach majority fixation in the fifth wave - again showcasing how the quasispecies mutant swarm will invariably change its shape over time, and depending on the challenges its facing.

So in the many months since the COVID-19 Pandemic began, it’s abundantly clear the people who started it and are profiting the most from it have instructed the media not to talk about “serial passage” at all, nor the past links to vaccine research and past viral outbreaks, including the 1977 H1N1 outbreak linked to military vaccine gain-of-function work as well as the 2009 H1N1 endemic, both likely from serially passaged LAVs that were able to make their way back to full strength much faster than the scientists who designed them anticipated. 

And so the silence from absolutely everyone when it comes to the connections our ongoing pandemic might have with vaccine research and serial passage is mirrored by the media’s refusal to discuss the millions and millions of culled farm-minks as a link to the obvious intermediate animal host. Since mink point directly to lab ferrets, their very close cousins, which were used during the 2012 gain-of-function experiments that led to a moratorium against the practice, and were almost certainly used to attenuate the SARS-like LAV, that would emerge at the Wuhan Military Games as SARS-CoV-2 - ferrets are the go-to animal to use for airborne vaccine work. 

Which is why this novel virus was able to create a second simultaneous pandemic across mink farms all across dozens of nations on multiple continents, because the virus was still incredibly well-acclimated to their physiology, since it so closely mimics the ferrets that the virus was serially passaged through as it was attenuated and weakened down into a LAV - appearing to the scientists building it to lose its FCS at some past point along the way, when in reality it was always there, hiding and waiting for when its unique ability might be needed to smile on humanity. 

And it’s almost certainly the past reversions of H1N1 LAVs in 1977 and 2009 that seemed to eventually just melt away, which sociopaths like Richard Ebright and the rest of his sweaty socially-retarded buddies at JASON are using to assure everyone that SARS-CoV-2, another LAV that’s reverting, will just melt away in just a few more months - just like H1N1 seems to have done twice. Unfortunately, unlike their mythical buddy: Each and everyone one of these arrogant old hacks was drawn into the siren song of multi-billion dollar defense and pharmaceutical contracts long ago, and they’re going to remain pushing for a fascist and entirely ineffective vaccination program because they’re rotten, filthy, diseased whores, and that is exactly what they are being paid to do. 

Our novel coronavirus is not a naturally spreading and evolving virus, and it has not become endogenous to human populations after thousands of years of coevolution - it is reverting back towards a highly-pathogenic SARS-like chimera that our immune systems will be entirely helpless against, and is going through the same unexpected epistatic gatekeeping mutations that OPV does on its way back to full virulence, which vaccines are also entirely helpless against. 

In the case of SARS-CoV-2, this gatekeeping results in the sudden emergence of new strains that appear evolutionarily impossible - like Omicron.  And so long as transmission is ongoing, there is nothing that is going to stop this pandemic except more death, because transmission means more gatekeeping, and gatekeeping means continued steps closer to the original strongest version of this highly-pathogenic virus. 

Being completely and entirely acclimated to the human genome is not at all the case with OPV, a LAV against the Polio virus that’s reverting all across the third world and bringing back Polio’s terrible paralytic poliomyelitis. So OPV serves as a much more accurate analogy for SARS-CoV-2 than the H1N1 LAVs.

Our novel coronavirus is a LAV derived from the work being done at UNC, the only place on earth trying to make a LAV for SARS-like viruses, which are also obviously not going to be fully acclimated to the human genome like the human influenza virus, which seems to have been with us at least since the Trojan War thousands of years ago. 

Until SARS-CoV-2 is understood as a LAV that’s deattenuating towards a highly-pathogenic chimeric coronavirus that’s going through gatekeeping mutations and has no intention whatsoever of following the assumptions drawn from observing natural evolution or even the paths of the H1N1 LAVs which melted back into their original endogenous human hosts - humanity is going to continue to be standing on its head as it attempts to battle this pandemic, and misunderstanding the basic fundamental nature of what its up against. 

It’s something we seem to be particularly good at, since all the way back in 1977 when the first H1N1 LAV emerged to a mass global panic, a massive push was made to create and distribute vaccines against what was thought to be a potentially pandemic strain. But it turns out that one of the ways a LAV isn’t a natural virus, is that when you attempt to vaccinate against it, neurological side-effects appear to proliferate among the vaccinated population, as the virus blows through this attempt at protection. 

Because unfortunately for all of us, this isn’t the first time we’ve all been down the horrific rabbit-hole of trying to rush out an incredibly profitable vaccine against an enigmatic mystery virus that’s really a military LAV that deattenuated faster than expected. A vaccine which only provides only weak and temporary protection - but also causes wide-spread side-effects because it turns out the pharmaceutical companies were lying about their vaccine studies, and knowingly risked the lives and livelihoods of tens of millions of Americans so they could make as much money as quickly as possible:

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