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means is that they actually looked at a mere thirty-seven primers out of the way, this is also how scientists characterized
the approximately thirty thousand base pairs claimed to be the genome the measles “virus”—by consensus!)
of an intact virus. The real blockbuster finding in this study
Next, the virologists took these thirty-seven segments and put them comes later, however, a finding so shocking that
into a computer program, which filled in the rest of the genome. This it is hard to believe what we are reading. Sum-
computer-generation step—called “whole genome sequencing”—con- marizing their procedures in the paper’s Results
stitutes scientific fraud of the highest order. section, the authors explain that they “examined
Here is an equivalency: A group of researchers claims to have found the capacity of SARS-CoV-2 to infect and rep-
a unicorn because the group has a piece of a hoof, a hair from a tail and licate in several common primate and human
a sliver of a horn. After putting that information into a computer and cell lines, including human adenocarcinoma
programming it to re-create the unicorn, they claim that this computer cells (A549), human liver cells (HUH7.0), and
re-creation is the real unicorn. Of course, they have never actually seen human embryonic kidney cells (HEK-293T),
a unicorn, so they could not possibly have examined its genetic makeup in addition to Vero E6 and Vero CCL81 cells.”
to compare their samples with an actual unicorn’s hair, hooves and horn. Their aim was to monitor “cytopathic effects”
In the case of SARS-CoV-2, the authors of the June study report that they (CPEs)—meaning structural changes in host
decided on the virus’s real genome by “consensus”—in other words, by cells caused by “viral invasion”—where the
vote. Because different computer programs will come up with differ- infecting virus causes either lysis (breaking
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ent versions of the imaginary “unicorn” (virus), scientists have to come up) of the host cell or, if the cell dies without
together as a group and decide which is the “real” imaginary unicorn. (By lysis, an inability to reproduce. Both of these

isolated virus—just messed-up cells. As for the second approach, Wikipedia acknowledges that electron microscopy
also has shortcomings. Negative-stain electron microscopic examination may allow for “rapid visualization of poxvi-
ruses,” but it “does not allow specific verification of virus species or variants.”
The entry describes “virus isolation”—the third technique—as “the ‘gold standard’ against which other methods
of virus detection are compared.” This is true; virus isolation is the gold standard. Wikipedia continues, “Theoreti-
cally at least, a single viable virus present in a specimen can be grown in cultured cells, thus expanding it to produce
enough material to permit further detailed characterization.” Theoretically, yes, but in practice, pure virus introduced
into animals or animal cells has little effect. Only “virulent virus” will appear to multiply and cause disease.
These challenges explain why scientists readily use molecular methods such as polymerase chain reaction (PCR)
and real-time polymerase chain reaction assays, which Wikipedia credits with “faster and more accurate methods
of myxoma virus identification.” The site explains that “Real time PCR simplifies the diagnosis of myxomatosis by al-
lowing nasal, ocular, or genital swabs to be quickly tested.” Wikipedia does not mention the fact that PCR does not
identify specific viruses, only snippets of genetic material. So, while this method may be “faster,” it is certainly not
“more accurate.”
Even if scientists do isolate pure virus, they still need to show that this pure virus can make healthy rabbits sick.
Yet we don’t need an “infectious virus” to explain myxomatosis. During the 1950s, myxomatosis was intentionally
introduced in Australia, France and Chile to control wild European rabbit populations. Brought to these countries in
the eighteenth and nineteenth centuries to serve as a food source, and having few enemies, these rabbits bred like
. . . like rabbits. . . and soon overwhelmed the countryside, eating every green thing in sight. Did scientists kill them
off by introducing pure isolated virus or even “virulent” virus into the rabbits? No; they introduced fleas. The fleas
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dutifully bit the rabbits and myxomatosis followed, killing off huge numbers. Blood-sucking insects like fleas, mosqui-
toes and ticks contain an enzyme called apyrase in their saliva, which prevents platelet aggregation (clotting) at the
site of the bite. Apyrase keeps the blood liquid until the insect has had its fill. In animals that are breathing bad air in
overcrowded warrens, are undernourished due to scarce food (including clot-promoting vitamin K in green fodder)
and then are bitten many times, the enzyme can overwhelm blood-clotting capabilities and act as a poison. In short,
fleas and mosquitoes are one of nature’s ways to control overpopulation in various species of animals, and they do
it by poisoning them.
Likewise, we don’t need to call on “infectious viruses” to explain human diseases like TB in the Inuit or cholera
among the Chinese. Nutrient deficiencies, crowding and filth are perfectly capable of causing suffering and death
without the help of “viruses.” Finally, are researchers seeing “viruses” in their swabs and isolates, or helpful exosomes
which multiply in situations of stress and disease?

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