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Unnatural origins of Covid

and its Variants |
10-13 minutes

Covid and Its Variants are Laboratory

Creations
On September 4, I reported that Japanese
scientists had examined Covid and its
variants and found that all are Laboratory
creations. https://www.paulcraigroberts.org
/2023/09/04/japanese-scientists-find-that-
covid-19-and-all-of-the-variants-are-
laboratory-creations/ This discovery raises
the dangerous and disturbing question why a
laboratory is producing viruses with which to
infect humans.
I contacted a scientist who had been involved
in the study of the original SARS for his

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evaluation and explanation of the Japanese
scientists’ report. His explanation is below. It
is challenging for non-professionals to follow,
but less so than the Japanese study itself. As
I understand the findings, it is the absence of
synonymous mutations in the variants that
reveal that Covid and its variants are lab
creations.
I suspect that the Japanese study will be
suppressed and that any American or
Western scientist who took up this inquiry
would find himself cut off from research funds
and his career terminated.
Unnatural origins of Covid and its Variants
Marc G. Wathelet, Ph.D.
The origin of SARS-CoV-2, the etiological
agent of COVID-19, remains controversial
more than 3 years after its identification. Is
this virus the product of a natural zoonotic
event at a meat market in Wuhan or does it
come from a laboratory working on
coronaviruses? These two hypotheses are

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currently unresolved but a recent preprint
sheds much light on the issue, and raises
some troubling questions.
This preprint “Unnaturalness in the evolution
process of the SARS-CoV-2 variants and the
possibility of deliberate natural selection”
(https://zenodo.org/record/8216373), by
Atsushi Tanaka and Takayuki Miyazawa from
Osaka Medical and Pharmaceutical
University and from Kyoto University, was
written for scientists. Here is an attempt at
making their findings accessible to a larger
audience.
Their analysis of Omicron variants led them to
the conclusion that “the formations of a part of
Omicron isolates BA.1, BA.1.1, and BA.2
were not the products of genome evolution as
is commonly observed in nature.” How did
they come to such a startling conclusion?
They started their work by analyzing the
sequence of the Spike protein from a number
of isolates of the virus.

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A protein is a chain of amino acids that folds
itself into a 3D-structure and it is the
sequence of amino acids in that chain and the
shape of that structure that determine the
biological activity of a protein. In the case of
Spike, the main biological activities are
binding to a receptor at the cell surface and
allowing the fusion of the cell and virion
membranes, leading to the entry of viral RNA
into the cell.
The sequence of amino acids in a protein is
determined by the sequence of the mRNA
encoding it. This chain of amino acids is
produced by a specialized machinery in our
cells, the ribosome, which translates the
genetic information contained in the mRNA
nucleotide sequence into an amino acid
sequence.
There are four nucleotides in an mRNA
sequence, A, C, G and U, and there are 20
amino acids in proteins. How do we go from 4
nucleotides to 20 amino acids? Enters the

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genetic code, elucidated in the early sixties.
An mRNA sequence is read in triplets of
nucleotides, called codons. Because all 3
positions of a triplet can be any of the 4
nucleotides, there are 4 x 4 x 4 possible
codons, thus 64 codons total.
There is some degeneracy in the genetic
code, a given amino acid can be encoded by
1, 2, 3, 4 or 6 codons. For instance the amino
acid glycine can be encoded by these four
codons: GGA, GGC, GGG and GGU, which
brings us to a key concept, synonymous and
non-synonymous mutations. Genetic
sequences naturally varies over time, specific
nucleotides change, or are deleted or
inserted, these are called mutations relative
to the original sequence. RNA viruses in
particular are prone to rapid mutations.

When the 3rd nucleotide in a triplet encoding

glycine is substituted by any other nucleotide,
the amino acid encoded will still be glycine, it
is called a synonymous mutation. However if

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any of the first two nucleotides are modified,
the amino acid produced will be a different
one, it is thus a non-synonymous mutation.
Given the genetic code, a little less than a
quarter of random mutations will be
synonymous.
When a mutation is synonymous, the amino
acid is not changed and thus the activity of
the protein is not affected. For non-
synonymous mutations, the effect of the
changed amino acid can be unfavorable,
neutral, or favorable for the function of the
protein. Most non-synonymous mutations
negatively affect the performance of a protein,
because a protein sequence is already the
product of a long evolution selecting favorable
amino acids.
In the case of a virus, unfavorable mutations
are at a disadvantage and quickly eliminated,
it is negative selection, while favorable
mutations have a competitive advantage over
no or neutral mutations. For instance

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mutations that would increase the affinity of
Spike for its cellular receptor are favorable
and are positively selected. After this basic
molecular biology introduction, we are now in
a position to understand the data presented
by the Japanese researchers.
They examined 3 Omicron lineages, BA.1,
BA1.1 and BA.2. Compared to the original
Wuhan strain, BA.1 has 50 amino acids
changes, 39 of which were found in Spike,
which is a 1,273 amino acid long protein, out
of the 14,149 amino acids encoded by the
virus. It is expected that more mutations are
found in Spike compared to the rest of the
genome, because of the constraints against
change to maintain function for the replication
machinery (11,501 amino acids) and the
selective pressure on Spike to better interact
with its receptor.
Omicron BA.2, identified less than 2 weeks
after BA.1, has 31 amino acids changes
compared to the Wuhan strain in Spike, 14 of

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which are shared with BA.1. Uncannily, these
early Omega Spike sequences have a single
synonymous mutation and 39 or 31 non-
synonymous mutations for the BA.1 and BA.2
lineages, respectively. This ratio of
synonymous to non-synonymous mutation is
clearly abnormal as ~24% of random
mutations are expected to be synonymous
and generally there is no selective pressure
for or against synonymous mutation.
By contrast, immediate descendants of BA.1,
such as BA.1.1, BA.1-0.1, and BA.1-0.2 have
23 synonymous mutations and BA.2-01, the
immediate descendant of BA.2, has 21
synonymous mutations, but no new non-
synonymous mutations. Synonymous
mutations are known to accumulate regularly
over time, providing a sort of evolutionary
clock, while non-synonymous mutations
accumulation is a function of their benefit to
the virus replication.
The BA.1 and BA.2 lineages must share a

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common ancestor given their 14 identical
non-synonymous mutations and one
synonymous mutation in Spike, and from the
time of their divergence, many months must
have elapsed in order to accumulate an
additional 25 or 17 non-synonymous
mutations, respectively. Yet, during that time,
some 8-10 months, not a single synonymous
mutation occurred in either lineage, which is
clearly incompatible with natural evolution
and with the observation that their immediate
descendants harbored over twenty
synonymous mutations in their Spike
sequence.
What about the earlier variants? Compared to
the original Wuhan strain, the Alpha variant
had 10 non-synonymous mutations in Spike,
Beta had 10, Gamma had 12, Delta had 11
and Mu had 9, but strikingly none of these
variants had any synonymous mutation in
Spike. Such observations are unprecedented
in the history of natural viral genome

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evolution.
Back to the Omicron lineages, the
researchers probed databases looking for the
immediate precursors of BA.1 and BA.2. To
do this, they started by reverting one of each
changed amino acid back to the original in the
Wuhan sequence and used an alignment
program to find perfect matches in the
databases. According to evolutionary theory,
one would expect to find variants where one,
two, three and more of the changed amino
acids correspond to the original Wuhan
sequence.
Such climbing back of the evolutionary tree
would identify the path followed from the
common ancestor to BA.1 and BA.2,
progressively accruing additional changes in
their amino acids sequence, but this is not
what they observed. Astonishingly, they found
100% matches for 38 of the 39 single
reversed amino acids of the BA.1 lineage.
Likewise, they found perfect matches for 29

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of the 31 reversions found in the BA.2
lineage.
These results could not be more incompatible
with evolutionary theory, where we expect the
progressive accumulation of changes in
amino acids sequences, and not what is
observed here, 38 and 29 candidates as
immediate precursor of BA.1 and BA.2
lineages, respectively.
It is possible that some of these sequences
could be what is known as natural revertants,
where a new mutation restores the mutated
amino acid back to its original identity.
However, such rare reversion events would
need an astronomical number of sequences
to be probed in order to detect them all, and
the limited number of sequences present in
databases exclude that possibility.
How do we account for these observations,
then? A molecular biologist will recognize this
pattern of mutants as that of a classic
experiment where the effect of specific

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mutations is systemically analyzed, one by
one. Alternative hypotheses, based on natural
evolution, do not come to mind.
The most parsimonious hypothesis to account
for the observations reported by Tanaka and
Miyazawa is that the Omicron lineage BA.1
and BA.2, as well as all their single amino
acid revertants found in databases, are
specifically designed and generated
laboratory products.
Moreover, the grossly abnormal imbalance
between synonymous and non-synonymous
mutations found in the Omicron BA.1 and
BA.2 lineages is also found in the Alpha,
Beta, Gamma, Delta and Mu variants, which
each have about 10 non-synonymous
mutations but zero synonymous changes in
nucleotide sequence. Because the probability
of such a mutation pattern is exceedingly low,
it is difficult to escape the conclusion that
these variants are most likely laboratory
creations as well.

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The implications of these findings on the
origin of SARS-CoV-2 are sure to be
profoundly disturbing.

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