(WMR) -- A
virologist who has been researching the A/H1N1 virus has concluded after months
of research that the �novel� influenza was re-assorted in a laboratory
from eight genes consisting of avian, swine and human type influenza A
The scientist does not believe, based on intensive
laboratory research of the A/H1N1 virus, that its sudden appearance in Mexico
this past spring was a natural occurrence.
The reassortment of viruses occurs when one or more complete
genes are exchanged enabling the virus to adapt to a new host. An example is
when the avian virus switches gene with a human virus. In the case of A/H1N1,
three genes were exchanged, from avian, swine, and human influenza viruses,
resulting in the ressortant virus now expected to launch another deadly wave of
infections in early October.
There are also signs that adaptation leading to
mutation has occurred in the A/H1N1 strain. Several cases of mutated
A/H1N1 have been reported from around the globe, rendering treatment with
anti-A/H1N1 drugs and A/H1N1 vaccines ineffective.
Adaptation takes place when a small change takes place in
the virus and sometimes that can be one amino acid alteration. The adaptation
permits the virus to thrive in its new host. A/H1N1 is believed to be a
laboratory strain because a specific amino acid was discovered that appears to
have made several passages in eggs. The vaccine industry usually amplifies
viruses by isolating them in eggs and after several passages, the mutation
can be discovered.
The mutation of A/H1N1 has been discovered by our virologist
source to have been more rapid than is naturally possible. The following is
what was described in scientific terms about the rate of mutation of A/H1N1:
�Mutation takes time to occur, up to the rate of amino acid
substitution. For example, for HA gene, or �duck virus,� HA has a substitution
rate about 3 x 10e-4 per site per year which is slower compare to human and
swine HA (about 10e-3 per site per year). If the total nucleotide number
in influenza A virus HA is 1,700, then it takes three years for
making a single change in the duck virus, or 1.7 year in the case of
human and swine virus.�
The natural rate of mutation for a complete gene
mutation, according to the virologist, takes �thousand of years to be
As far as the reassortant A/H1N1 virus is concerned, there
is a fear that a human was used as a laboratory �guinea pig� to permit the
exchange of genes between humans, pigs, and fowl. The reasoning is that an
individual was infected by avian, human and swine virus simultaneously,
and the viruses exchanged genes inside the individual�s body, creating a new
virus having mixed genes and then rapidly spreading to others.
Herein lies the suspicions concerning the purposeful
creation of A/H1N1 and its infection of a human host.
WMR�s virologist source stated, �The host should have
efficient receptor for those three different derived hosts. So far, human virus
tends to infect humans, because it is suited to a human receptor. Avian virus
tends to infect birds, because it is suited to bird receptors. Pigs have both
human and avian type receptors, so it is believed that pig serves
as the �mixing vessel.� However, some researchers tried to prove the �mixing
vessel� theory by trying to infect pigs with human and avian viruses to
create a reassortant virus.�
The test involving the infection of pigs with reassortant
human and avian viruses failed.
While it is common for pigs to become infected with human
and avian viruses, there are no reports that pigs shed the reassortant A/H1N1
virus and infected new hosts, either human or bird.
What is known is that the first A/H1N1 virus was found
in a human. Although some pigs and turkeys were infected with the A/H1N1 virus
by farm workers, there is no evidence that the opposite occured.
Reassortant genes also require ancestor viruses. According
to the virologist, �If you check the phylogenetic tree, it shows the NA
and M genes derived from avian virus, PB1 from human H3N2; other genes (PB2,
PA, HA, NP, NS) from swine triple reassortant, swine H1N2 and Eurasian swine
(H1N1/H3N2). The triple reassortant swine actually derived from human H3N2
which infected pigs, and has been circulating in North America for at least 20
years. When people say it is �swine virus,� it�s actually human virus.�
It has also been discovered that suspected ancestor
viruses are coming from old isolates. The NA gene comes from a 1996-2001
isolate, the M gene from 1990-1993 isolates, and the others even older,
somewhere between 1979 to 1980�s isolates. The consensus virologist community
contends that the A/H1N1 virus has been in existence for over 20
years without ever being detected. WMR�s virologist states that it is
impossible for a virus existing for 20 years without being detected given the
amount of virus medical surveillance that takes place around the world.
The virologist has not detected any evidence of 1918
influenza RNA/DNA in A/H1N1. However, the 1918 flu, like A/H1N1, began in a
first wave in the spring and came back with a vengeance in October. The 1918
flu killed an estimated 50 million people around the world. Although no genetic
evidence of a link to 1918 flu has been discovered by the virologist, the same
scientist who has conducted research into A/H1N1 and may have received DNA
samples from the buried corpse of an Inuit woman in Fort Brevig, Alaska, who died
of the pandemic in 1918 is also financially linked to an A/H1N1 vaccine
The virologist has asked an alarming question about
A/H1N1,�How can you mix avian, human and pig virus at one time? The viruses
must have come from Europe, America and Asia, without any detection?�
The virologist adds, �The virus emerged suddenly in Mexico.
I can�t explain how. I wish I could. For me as a virologist, it�s impossible . .
. on the other hand, technology can create any kind of virus you want.�
in the Wayne Madsen Report.
Copyright � 2009 WayneMadenReport.com
Madsen is a Washington, DC-based investigative journalist and
nationally-distributed columnist. He is the editor and publisher of the Wayne Madsen Report