Coaxing Viruses into Existence

By Julie Beal

The technocrats must be creaming their pants with delight … thanks to the no-virus theory, they’re getting away with the biggest heist in history. Evidence suggests that a relatively harmless virus called SARS-CoV-2 was designed and released for the Reset. All eyes should be on that super-special spike and the way it fits so well with the vax that were ready and waiting by 2019, but the no-virus theorists wave their hands and say, ‘Nothing to see here, folks!’, and everyone looks away. It’s like a dream come true for Big Pharma, too, coz we’re not supposed to mention viruses any more. It’s reached the point where it’s now wrongthink to even wonder about the existence of viruses because, of course, ‘there’s nothing there’. What’s to talk about if viruses don’t exist?

And yet … there are so many things their theory doesn’t explain, especially when it comes to vaccines. If viruses don’t exist, what are the adenoviruses in the AstraZeneca vax? Do they cause disease? What about warts and cold sores? How does anyone know what a spike protein is? Why are people getting shingles after the jabs? How did Dr Wimmer make a poliovirus using the chemical formula C332,652H492,388N98,545O131,196P7501S2340? What can we learn from the Cutter Incident? How can viruses be patented if they don’t exist?

A no-virus theorist would probably dismiss these questions by saying viruses can’t exist because, they reason, they’ve ‘never been isolated’. However, they use a dictionary definition of isolation, confuse it with purification, and never explore the proof of the pudding, which is replication. Only by uncovering what virologists mean by these terms can we arrive at some kind of answer as to whether or not something has been found, rather than created, and whether or not we can call it a virus.

Along the way we might find that something very small was found, and, with gentle encouragement, an army of clones could be created. Coaxed into existence, the clones could be moulded, mutated and trained into being what virologists think they should be.

You say this word ‘isolation’ but I don’t think you know what it means

Sometimes ‘isolation’ just means ‘separation from the group’, and when virologists use the term, sometimes they just mean ‘separation from the host’ and/or ‘separation from the host cells’. Most of the time, though, when virologists say they’ve isolated a virus, they mean they did the separation part and then proved it by getting particles to grow in a cell culture. When particles ‘grow’ in a cell culture like this, it’s because they are replicating, i.e. producing multiple copies of themselves. It’s then possible to confirm the particles are replicating by taking a small sample from the cell culture and adding it to a fresh one to see if the same kind of particles continue to be produced. This process can be repeated from one cell culture to the next, which shows that something is being ‘carried over’ each time. The no-virus theorists say the particles coming out of cells are either exosomes or fragments of dead cells, but these components are unable to replicate, so if any exosomes or other cellular material are ‘carried over’ along with the viruses, they won’t make a noticeable difference to the final harvest, because only the viruses multiply.

The no-virus theorists also claim that virologists poison cells when in fact they use standard protocols for keeping cells alive, so in the end their theory falls apart, and all they have left is the claim that Koch’s Postulates have not been fulfilled, which makes sense when questioning the ability of a virus to spread disease, but not when questioning the existence of viruses as biological constructs. Things can exist without being pathogenic.

Still, it’s hard to get your head around the idea that anything that comes from a cell culture could possibly have anything to do with something on a nasal swab. This is why replication is so important – it tells us a great deal about the molecular changes that occur when viruses go from one type of cell to another, e.g. from a cell culture to a human being, or from an animal to a cell culture. Examining these changes can help us decide whether or not there ever was a virus on that swab, or in any other sample from a person who ‘tests positive’.

The meaning of ‘isolation’ keeps changing

To work out for yourself whether or not viruses exist, it helps to understand what virologists mean when they say they’ve isolated a virus, and how this meaning has evolved over time. Bear in mind that the ability to cause disease may depend on the type of virus, as well as the dose given. This may be considered as evidence of an association with that disease but it doesn’t tell us how the virus came to exist in the first place.

The early history of virology has been agreed upon ‘with hindsight’, but it’s said to have begun with the isolation of the tobacco mosaic virus in the late 1800s. A scientist called Iwanowski discovered he could filter an invisible substance from diseased tobacco plants and use it to spread the same disease in healthy ones. Scientists were excited by this discovery because disease was rife, and they’d already pinned some of these diseases on various types of bacteria that could be isolated and cultured in the lab, so they were obsessed with hunting microbes and proving contagion as a way to explain why so many people were ill. A lot of people were suffering from a disease called polio, so they wondered if it might be caused by the same kind of invisible substance that seemed to be in the tobacco plants. In 1908, Landsteiner and Popper used the spinal cord of a young boy with polio to perform experiments on two monkeys. The boy had died after developing paralysis four days earlier, and a filtered sample of his spinal cord was injected into the two monkeys. They both became paralysed and died, and they had the same kind of lesions in their spinal cords as the boy. Subsequent experiments by other scientists got the same results, and many of them were funded by the Rockefeller Institute. In 1910 (the same year the Flexner Report was released), Rockefeller scientists announced they’d found neutralizing antibodies to polio in the blood of monkeys.

From this point on, a virus was defined as a filterable poison that transmitted disease and caused the production of antibodies. Isolating a virus involved filtering the body matter of a person or animal suffering from a particular disease and using it to create a similar disease in another animal. Body matter from this animal could then be filtered and used to cause the disease in another (healthy) animal. The process could then be repeated in other animals, which led to the assumption that viruses were contagious disease-causing organisms, just like bacteria.

It wasn’t long before the definition of isolation moved on again, when the invention of the electron microscope[i] and the development of tissue cultures managed to make things visible. Thus, from the 1950s onwards[ii], viruses were defined as filterable particles that were, i) capable of replication, ii)  associated with the production of antibodies, iii) visible with an electron microscope,[iii] and, iv) able to cause cell death in a tissue culture.

But things really moved on with the advent of genetic sequencing. It changed the game forever because it revealed the existence of many thousands more viruses in every square inch[iv] of the earth, most of which are harmless. However, it also allowed scientists to characterize viruses in such minute detail, they could create them from scratch. In 2002, Dr Wimmer made the news when he demonstrated that a poliovirus could be understood as a chemical, and he managed to stitch together all the genetic molecules that make up the poliovirus, and then used it to paralyse and kill a bunch of mice. (But he did have to use a high dose!)[v]

Characterizing viruses according to their genetics is now standard practice for virologists and vaccine manufacturers and there’s a lot of useful info to be gleaned from their experiments. They provide highly specific, forensic details about what happens when a virus is transferred from one cell culture to another, or from a cell culture to a human or animal. Sequencing shows that replicated particles aren’t always faithful copies of the ones that preceded them, because there are usually small genetic changes each time they go into a different cell type. However, the changes are small and few in number, which suggests that the very first particles that grow in a cell culture when a patient sample is added to it may in fact be a fairly good representation of something that was contained in that sample.

Encouraging viruses to multiply

Viruses have always been coaxed into existence by practitioners of virus production. They start out with something very small, focus in on it, then make a load more by using a bunch of cells of some kind. Human interference has an effect at every stage:

Step 1: Selection – the particles selected by the virologist are the ones that will be cloned. They always favour the ones that do damage to cells, i.e. cause a cytopathic effect. It’s like taking a snapshot of a moment in time… and preferring potential killers.

Step 2: Amplification – this creates a lot of lookalikes; viral particles keep on replicating themselves when added to a cell culture … so it’s like printing out loads of pictures that look very similar to the original snapshot (i.e. virtual clones of the cytopathic particles).

Step 3: Training – also known as passaging, this is the longest and most influential stage of the virus creation process because it involves forcing the lookalike virus to adapt to its new home, which is often a totally different species (i.e. a non-human host). For the virus, it’s almost like moving to another planet, it’s so different to the place it came from. It has to try really hard to fit in, and the end result of this is usually insertions, deletions or mutations in one or more places in its genome. Viruses mutate all the time anyway, but these kinds of mutations are all a result of their struggle to adapt, and they help viruses to keep on growing in the new cell-type.

Cell Culture Adaptations

The changes that take place when a virus is transferred to a new cell-type are referred to collectively as cell culture adaptations. The nature and number of the changes that occur are studied extensively because they’re the bread and butter of gain-of-function experiments and recombinant vaccine production.

Passaging and Attenuation

Whether they use live animals or cell cultures to grow viruses, virologists often struggle to get viruses to behave like they expect them to, in terms of the disease they’re thought to cause, so they experiment with various different cell types to get the effect they’re after, often using passaging techniques. Passaging involves allowing the virus to grow in a cell culture (or animal), then taking a sample and transferring it to a new cell culture (or animal) of the same type, allowing it to grow again, and then transferring it to yet another new set of cells. This process can be repeated umpteen times but, “a virus can typically adapt to a new host within ten or so passages”. Passaging often results in tiny changes to the virus genome which are said to attenuate the virus, i.e. make it less pathogenic in humans. This is considered desirable for vaccines because the attenuated virus is classed as being ‘safe enough’ for most humans whilst still inducing the production of antibodies.

An extreme example of the passaging technique was seen with a particular strain of H1N1 that was used for a flu vax in the 1940s. The virus was isolated in Puerto Rico in 1934 and multiplied happily when grown in fertilized chicken eggs, which meant huge amounts of virus could be produced for a vaccine. This flu virus was subjected to, “a very long adaptation process involving 77 passages in mice; 717 passages in cell culture; 30 passages in chick embryos; five passages in ferrets; and an additional 50 passages in chick embryos.”

In 1951, Hilary Koprowski created an oral vaccine containing live poliovirus that could replicate in the stomach. It was passaged up to 35 times in cotton-rats to attenuate it, and then fed to 18 children and 2 adults on a spoon; the vaccine, “consisted of 10 ml of 20% suspension of cotton-rat brain and cord infected with TN strain”. Koprowski also passaged another type of poliovirus, called the SM strain. Attempts were made to attenuate the virus by performing, “alternate passages in chick embryo and cultures of monkey kidney cells”, but it could cause neurological problems so, “a substrain called SM-N90 was passed 4 times serially in humans by oral administration of filtered fecal virus, isolated after replication in the intestine. After the fourth human passage, the virus was plaqued 4 times (“plaque purification”) in cultures of monkey kidney cells, and the resultant strain was renamed CHAT, after the name of the baby in whom the last human passage had been made.” The baby’s name was Charlton, and the fact that he was made to swallow live virus and human waste is just one small example that illustrates the degree of human interference in viral evolution at a time when ‘biosafety’ was only a loose concept. H V Wyatt[vi] explored this issue when he suggested that an epidemic of polio in New York in 1916 could have been caused by a lab leak from the Rockefeller Institute where Flexner and colleagues were trying to make poliovirus more pathogenic by, “passaging spinal cord tissue containing poliovirus, from one Rhesus monkey spinal cord to another. They had been unable to infect monkeys by feeding. These experiments continued with the passage virus which at times was reinforced with newly acquired virus from patients. When tested in 1936 by Sabin and Olitsky, this Rockefeller “MV” strain would replicate only in monkey neural cells, and no other.” The MV strain was also tested as a vaccine, and it’s now known that vaccine viruses can recombine with ‘natural’ viruses and evolve into something new.

Host Restriction

Virologists say the reason it’s hard to get viruses to grow in cell cultures is due to ‘host restriction’, i.e. viruses can only grow in certain species, depending on their particular genetic components and preferred molecular interactions. Each virus is said to have a particular ‘host range’, i.e. there’s a limit to the kind of cells or organisms it can replicate in. It’s the same with plant viruses, such as the tomato yellow leaf curl virus which can cause, “stunting, yellowing, leaf curl and flower senescence” in tomato plants, but has been confirmed by PCR to be present in other plant types, including cucumbers and peppers. It’s also said to demonstrate, “a positive interplay between viruses and plants” because it can also protect them against extreme drought.

Anyhow, SARS-like viruses are also subject to host restriction, as explained by Ralph Baric from the University of North Carolina: “SARS-CoV does not replicate in the guinea pig, and replication in the ferret is limited, resulting in minimal disease phenotypes.” In other words, the SARS virus won’t grow in guinea pigs, it struggles to grow in ferrets, and it doesn’t really make them ill. This is thought to be due to the fact that SARS-CoV doesn’t bind to the ferret ACE2 receptor very well, so it rarely gets into cells and is therefore less able to multiply and cause damage. Baric goes on to explain the benefits of passaging viruses to try and create the alleged pathogenic potential of viruses like SARS: “Many human and animal respiratory viruses have been adapted to mice. This requires iterative [repeated] passage to select for multiple mutations that afford alternative species receptor usage, increased virus replication, increased yields/cell and enhance severe clinical disease outcomes.”

Baric asserts that his experiments with mice and coronaviruses are no threat to the public, because they tend to end up being less pathogenic: “Critically, no evidence link coronavirus in vivo mouse passage with increased human risk … serial passage in one species usually attenuates virus pathogenesis in the original species.” Bear this in mind for Omicron, the even less harmful version of SARS-CoV-2, because it appeared all of a sudden and bears all the hallmarks of having been passaged in mice, as if it came straight from a lab. Omicron is a mouse-adapted virus that suddenly jumped to humans despite the fact that viruses are said to remain within their restricted host range and rarely ‘jump’ from one species to another. So it’s worth pointing out here that the series of outbreaks over the last 20 years, beginning with SARS, were all blamed on animal viruses jumping from one species to another, just like the rona, and this is being used as an excuse to increase surveillance and control. We’re supposed to believe that viruses are now more able to jump species as a result of global trade, travel and climate change, but that viruses passaged through humans and animals in the early 1900s were not.

Recombinant viruses and humanized mice

In an effort to recreate the set of symptoms and clinical pathology they expect to see during animal experiments, virologists are always on the hunt for a more ‘robust’ animal model to test viruses on. Put another way, animals are a poor substitute for humans, and viruses behave differently depending on what host they’re in. What virologists want is to make each virus capable of infecting a specific type of animal and preferably to make it ill as well. If passaging a virus doesn’t work, they can use genetic engineering to make the viruses more infectious or virulent or some other quality by introducing tiny molecular alterations, e.g. to change the way the viruses attach to cells. Another thing they can try is to ‘humanize’ the animals by changing a part of their genome to be human-like, and again, this often involves changing specific cell receptors.

Ralph Baric and colleagues have spent decades trying to make SARS-type viruses more deadly to various types of animals, but they’ve not had much luck.

In fact, the only time Baric managed to make mice ill with SARS was when he created a ‘mouse-adapted’ version of the virus (called ‘MA15’) by passaging it fifteen times through mice. He used it to infect aged and ‘immunosenescent’ mice in an effort to “recapitulate severe lung pathologies” reportedly found in SARS patients, most of whom were elderly and/or had a weak immune system. (More on Baric’s experiments – and details about SARS patients – in future articles.)

Measles as an example of adaptation to tissue culture

Finding out what happens to viruses in tissue cultures can give us some idea about what might happen to a human virus that’s been propagated in animal cells of some description. Various different aspects of the way viruses respond to being put into different kinds of cells are described in a study called ‘Adaptation of Wild-Type Measles Virus to Tissue Culture’ (Waku and Wild, 2002) and summarized below:

  • The only living creatures the measles virus will grow in are humans and monkeys in captivity.
  • In the lab, the measles virus grows quite quickly in certain human and simian cell lines, but it takes a while to get the virus to adapt and grow in other types of cells. The researchers reckon this is to do with two particular cell receptors (CD46 and CD150).
  • As with some other viruses, measles takes different forms according to its geographic location (!), and, as is standard practice, the variations, “can be differentiated by nucleic acid sequence analysis”.
  • The measles virus (MV), “was initially passaged in primary embryo human kidney cells and then serially passaged in chicken embryo fibroblasts until it had an attenuated phenotype when reinoculated into children. During this adaptation, there were a number of mutations introduced into the MV genome. Among the properties associated with the vaccine virus was the ability to replicate in human and monkey epithelial and fibroblastic cell lines.”
  • “Whereas the virus can be rapidly isolated from clinical specimens in both human and monkey B-cell lines, isolation on epithelial cells such as Vero cells can take weeks and several blind passages.”
  • Adaptation to Vero cells may lead to a mutation of the amino acid at position 481.
  • The best way to make monkeys ill with measles viruses is to use viruses that have been grown in B-cell lines because they turn out to be both virulent and pathogenic, whereas growing them in Vero cells weakens (or ‘attenuates’) them and then they don’t make monkeys very ill.

Messing around with viruses changes the way they behave and can change the type of disease that manifests. As documented in ‘Dissolving Illusions, Disease, Vaccines, and the Forgotten History’, by Suzanne Humphries, MD and Roman Bystrianyk,  some people who received a measles vaccine in the 1960s went on to develop ‘atypical measles’ which was, “characterized by a higher and more prolonged fever, unusual skin lesions and severe pneumonitis compared to measles in previously unvaccinated persons.” The authors also note that, “measles vaccine virus can be detected in urine after vaccination” using PCR tests, and that an illness classified as ‘modified measles’ is linked to receipt of attenuated vaccine-viruses.

As described in previous articles, there is plenty of evidence that vaccine-viruses with specific genetic sequences can be shed from the body and transmitted to others. This is why some package inserts for vaccines contain warnings about it. Live viruses used in vaccines can recombine and evolve into mutants by exchanging genetic material with other, similar viruses. Viruses that were isolated from people suffering from vaccine-associated paralytic poliomyelitis (VAPP) were found to have recombined with both ‘wild-type’ viruses and other vaccine-viruses. For example, “vaccine-specific segments of the Sabin virus genome” had come to be replaced with non-vaccine sequences derived from wild polioviruses.

A study by Vega et al (Mutational dynamics of the SARS coronavirus in cell culture and human populations isolated in 2003’, 2004) analysed mutations that occurred in SARS viruses during human-to-Vero and Vero-to-human cell transitions. To do this, they isolated the virus directly[vii] from tissues taken from SARS patients and then sequenced them to get the ‘human version’. Then they used these samples to infect some Vero cells, and sequenced those isolates as well. In order to assess the effect of passaging, one of the samples was passaged five times (i.e. in five different Vero cell culures) and sequenced after each passage. Their results indicated that, “the transition from human tissue to growth in Vero cell culture” resulted in almost no changes to the genome at all, and they concluded that SARS-CoV barely ever mutates when grown in Vero cells. The isolate that was passaged five times in Vero cells showed there was only one amino acid mutation at position 18356.

The researchers also described how someone working in a lab in Singapore accidentally got infected with “a stable lab SARS-CoV isolate commonly used for in vitro experimentation”; they sequenced this isolate and then sequenced a sample of the lab worker’s sputum. The genomes were identical to each other, which meant the transition from Vero to human cells did not cause any mutations in this particular case.

But what about the mutations that could have taken place when scientists were using orphaned babies and animals in vaccine farms? Can we ever know what the ‘original’ virus was like? Meddling with viruses has unleashed mutants that may have warped our immunity:

As they evolve, so do we, so we are keeping pace with each other, on the whole. But when an anomaly comes along in the shape of a lab-created DNA construct, it takes us off guard. It’s as if it went off and gained strength and tactical cunning somewhere before coming back to launch an all-out strike. The strength comes from its ‘evolution’ to a new form which took place ‘elsewhere’, instead of on the battlefield, where we could witness it and evolve along with it. So it already has an advantage.

The reason we evolve together is because we are intricately connected – we share the same space. But if a virus goes to live in a bunch of HEK293 cells in a lab, it could allow it to develop in hitherto unseen ways. None of the media they use to grow viruses are the same as a human body, so the viruses that result are HEK293 adapted viruses, rather than modern-human adapted viruses, i.e. they become best suited to living in baby cells of the HEK293 variety. That’s not normal, and nor is it normal to have such unnatural constructs delivered directly into a vein.” 

Meddling with viruses led to the creation of mutant coronaviruses that paved the way for the Reset and gave rise to the monstrous plan to infuse the world with alien genetics and mutant spikes. People are dying. It cannot go on. We the people know this is wrong and the War for the World continues.


[i]   According to Stefan Lanka, “The electron microscopic photographs of the alleged viruses, for example, in reality show just regular particles of dying tissues and cells, usually at most in model form. However, since those involved BELIEVE that these dying tissues and cells are viruses, this dying of cells and tissues in the form of all kinds of cellular parts is also called the “multiplication” of viruses.”

[ii]   Some no-virus theorists claim virology began in the 1950s with the invention of cell cultures, and echo the ideas of Stefan Lanka, who formulated the no-virus theory in the late 1990s. When he issued his ‘prove measles exists’ challenge in 2011, one of the papers he was presented with was a paper by Enders et al describing the isolation of measles virus. In a recent video, Dr Kaufman described it as being, “the first paper published where they used the cell culture technique which later became known as virus isolation.” But virus isolation was already ‘a thing’, influenza viruses were being manufactured in fertilized chicken eggs, and, in the same year the measles paper was published (1954), Enders and colleagues received a Nobel prize for something they’d achieved in 1949, i.e. successful propagation of mumps, chickenpox, influenza and polioviruses using cell cultures. But this wasn’t the first time tissue cultures were employed by virologists. For example, in 1936, Rivers and Magill from the Rockefeller Institute used influenza virus, “derived from infected mouse lungs”, to inoculate a tissue culture consisting of, “minced chick embryo suspended in Tyrode’s solution”. The virus was passaged 160 times in just eleven months, and was tested on humans as a vaccine.

[iii]  Many viral particles look very distinctive (e.g. poliovirus and adenovirus).

[iv]  For example, “A teaspoon of seawater typically contains about fifty million viruses. Most of these viruses are bacteriophages which infect and destroy marine bacteria and control the growth of phytoplankton at the base of the marine food web.”

[v]  “To distinguish any synthesized viruses from lab contaminants, the investigators introduced subtle changes into the virus’ genetic code that didn’t alter the proteins it encodes. Unexpectedly, however, the newly created viruses turned out to be much less potent than the typical lab strain. Higher doses of the synthetic poliovirus were needed to kill mice, for example.”

[vi]   ‘The 1916 New York City Epidemic of Poliomyelitis: Where did the Virus Come From?’ H V Wyatt, 2011

[vii]  “SARS-CoV from the primary patient tissues were isolated by homogenizing the tissues in PBS buffer followed by a low speed centrifugation to obtain the viral particle containing supernatant.”

Read much more about the science behind the coronavirus injections at Julie Beal’s archive.

Image: Pixabay

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