Molecular Evidence for COVID-19's Engineered Origins
Maybe it’s time to take a moment with someone who was literally scrubbing prison toilets a few years ago, and yet can still easily explain how obviously engineered SARS-CoV-2 actually is.
1. Gatekeeping Mutations:
When the live-attenuated polio vaccine is working its way back towards being the full-strength polio virus (deattenuating, the opposite of “attenuating,” or weakening), something that often happens within communities that have poor sanitation, it goes through a series of coordinated changes. These coordinated changes are referred to as “epistatic” when the coordination is happening inside genomes, and it turns out these epistatic genetic changes are predictable, and unnatural when a live-attenuated vaccine (a weakened but not-quite-dead virus) is trying to work its way back to its original form. These mutations occur in a coordinated fashion in this circumstance, a coordination that does not show up in nature - as if the virus has a memory of being at its full strength, and is able to use epistatic mutations to make its way back to its original form far quicker than would occur naturally.
Not only does COVID-19 also display these coordinated, simultaneous, epistatic mutations across many different regions of the globe within human populations, these exact same mutations are also appearing in lab mice as well as on mink farms. There is absolutely nothing even vaguely approaching a natural parallel to this phenomenon, viruses do not use the same mutations to adapt to three different species simultaneously – different species require different mutations to establish active sustainable infections within a population, which is why diseases don’t just jump instantly and randomly between species, even ones living near each other.
So the fact that the exact same mutations which appeared in the UK and South Africa in humans, also appeared within the laboratory as COVID-19 was passaged through laboratory mice, is entirely unprecedented. And in mice, not only did repeated serial passaging make the same epistatic mutations that were seen in humans in the UK and South Africa appear, these mutations gave COVID-19 the ability to transmit through the air between the mice.
This kind of “gain-of-function” from serial passaging is a very direct sign of laboratory engineering, there is no natural way for the same mutations that cause a virus to become airborne between mice would also show up simultaneously in a human population as well as mink, or the population of any other discrete species. Different species require different mutations for a virus to adapt to it and establish active infections, that is why zoonosis is such a big deal.
2. Simultaneous International Pandemic Across Mink Farms:
When highly-pathogenic avian influenzas (HPAIs) jump off of poultry farms, they initially can never jump from person-to-person. Even with the constant exposure to chicken viruses that poultry farm workers get, they still need a lot of time for the myriad transmission events that are required before the virus can jump from human-to-human. And even when an HPAI does, it can never jump from person to person at first. After all, 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."
So the simple fact that COVID-19 immediately established human-to-human transmission is highly unusual and arguably a smoking gun on its own, but it’s much more extreme than that. Not only did human-to-human transmission immediately occur, so did human-to-mink transmission, followed by a mink-to-mink pandemic across over a dozen countries. Even when an HPAI jumps off of a poultry farm into its human workers, these viruses cannot pass from human-to-human at first. And they have absolutely never been demonstrated to transmit from human to another species – not even a close one like another species of bird, for instance.
For COVID-19 to be able to jump from humans directly into mink and start immediate pandemic transmission there, means that mink or a close relative must have played a recent role in COVID-19’s evolution. Mink and their cousins the ferret as well as humans all have similar respiratory systems, but not so similar that any other human virus has ever jumped directly between them before, nonetheless one also so well-attuned to both that it created instantaneous pandemics in each species – not just enough affinity to cause an infection in the lab, but so much that the virus accidently jumped into instantly into mink farms creating pandemics there across multiple continents.
No influenza or other virus has ever done anything like there, there is absolutely no other concrete demonstrable explanation in recorded history for this phenomenon other than passage through lab ferrets as well as humanized mice with human ACE2 receptor genes spliced into them. Mink and ferret can interbreed and are nearly the same species, and ferrets have been identified as the ideal animal for vaccine studies into respiratory viruses for years:
“Although different animal models are used in vaccine studies, the most appropriate model for studying SARS is ferret since it develops the typical clinical signs, viral replication patterns and lung pathology compatible with that of SARS pathogenesis in human.”
The first peer-reviewed science paper to discuss an engineered origin for COVID-19 was published August 2020 and written by a 40-year PhD in Microbiology who designed one of the most important genetic sequencing databases in existence decades ago and his son, neither of whom has ever worked for pharmaceutical companies or the private defense industry or foreign governments. The paper discusses the gain-of-function technique of serial passage as a likely source of the novel coronavirus. Using laboratory ferrets for vaccine attenuation would mean serial passaging the virus through them, so the virus would gain a high affinity for the ferret immune-system and intercellular environment, and ability to adapt to it.
This is a simple parsimonious explanation for COVID-19’s immediate jump into mink farms all across the planet, and the pandemic it caused there – COVID-19 was recently passaged through ferrets in the lab, as part of vaccine research. Every other explanation requires conjecture and leaps of faith. And serial passage provides a straightforward explanation for another highly unnatural characteristic for the novel coronavirus’s genome, that is much more definitive than the furin cleavage site.
3. The Canyon Hypothesis:
In the context of attenuating a potential vaccine candidate, serial passage can refer to the process of allowing the natural and expected mutations that diminish a virus’s virulence to occur—although in the unnatural setting of cell cultures or among caged laboratory animals—as a virus becomes acclimated to a new host species’ cells, which will have different receptor-requirements than its original host. Since ferret respiratory systems serve as workable analogues for humans in laboratory environments, they are an ideal animal to use if full “in vivo” host passaging is used between live animals, as opposed to “in vitro” passaging which is just between cell cultures.
Once this initial adaptation occurs, initially yielding mutations that can either increase pathogenicity in the new host or be deleterious to it, additional “passages” in the form of the virus naturally passing among new hosts (or among their cells in culture on a lab bench) will then slowly lead to a natural attenuation of the virus relative to its old host. This is why passaging can be used to attenuate and weaken a virus in the effort to create vaccine candidates that will elicit immune responses, but less serious infections.
And COVID-19 is unique in that it is the only human coronavirus in recorded history that violates the Canyon Hypothesis:
“Natural zoonosis means passing the challenges naturally posed by the immune system of a new host species; however, cellular serial passage can bypass these processes and create unique phenomena, possibly like SARS-CoV-2’s flat and non-sunken surface of its sialic acid-binding domain, which contrasts with the typical canyon observed in every single other ever observed coronavirus.”
Although it involves microscopic receptors and proteins, the process of a virus penetrating a cell is in fact a purely physical one that doesn’t involve chemical reactions. Part of accomplishing this penetration appears to be the formation of a physical dent, a canyon, in the surface of a virus that appears over time, as it learns to defeat the host immune defenses. Unlike every other coronavirus recorded however, COVID-19 appears to violate this rule and does not have a dented canyon on its surface. The only explanation for this is an artificial origin, relatively recent past serial passage through cells in vitro, which don’t present the full array of immune defenses as an entire live animal.
Any one of these three concepts alone is enough to act as a smoking gun for an artificial engineered origin for COVID-19, the fact that there are three complementary ones should leave no doubt about the novel coronavirus’s provenance, however it should make policymakers question why any scientist alive is acting as if there is still any debate at all. There is not.
COVID-19 was inarguably engineered in a laboratory.
H2BH -- have read your articles for the last year and appreciate your ongoing attempts to break things down critically. So let me ask a question as I'm curious what your view is....
This is the first time I've read an argument that COVID is a de-attenuating virus. So I'm curious how you reconcile this theory with suggestive evidence that fatality of the virus was higher in the past and then the circumstantial evidence the virus targeted women more virulently than men early on.
By the former I mean more than the early videos of people collapsing in the street, but also projections of the mortality rate as somewhere in the 1-2% range based on cases like the Diamond Princess. On the latter, there is the rumour that one of the earliest researchers to die was a young women, and then the suggestion from the Washington Post (?) that one of the early fatalities was the wife of one of the three WIV researchers who got sick. But now men are affected disproportionately it seems.
Wondering if you have any thoughts. How can a de-attenuating virus be both increasing infectiousness and danger and yet also losing those properties relatively quickly? What am I missing here?
I will never forget reading your first article in Sars-cov19 and thinking you are onto something. Here we are today and you were right all along. I guess the next question is the big one. Why was gain of function funding continued, the players involved, how was the virus released and why and who is profiting from this. Frightening.