I have taken relevant snips. It is a very long article with lots of scientific context, worth reading the whole thing if you have time. How long until this all comes out in the mainstream?
Harvard to the Big House: A Grin Without a Cat
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 its 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.
...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.
...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:
...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.
...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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