If
your understanding is the current H1N1 late-2009 season flu pandemic
began in Mexico as it spread from herds of pigs to humans there
you are probably among the millions who have been misled as to
the origins of this flu outbreak.
Only
one group of virologists that I could find has asked the right
questions and has properly investigated the origins of the H1N1
swine flu virus of 2009. Yet even these virologists are off the
mark when it comes to understanding the current flu pandemic.
Professor
Adrian Gibbs and Dr. Jean Downie, virologists writing
at the Institute of Science in Society, provide much of the
following data for the origins of the current late-season flu
outbreak that is sweeping the globe.
It
is easy to get confused when reading about H1N1 flu viruses. When
referring to H1N1 flu variants, these do not necessarily refer
to the triple reassortant H1N1 late-2009 flu virus that is completely
novel and unprecedented. The Spanish Flu of 1918 was an H1N1 flu
variant, but not the exact variant currently in circulation. These
flu variants need to be distinguished from each other.
Furthermore,
pay careful attention here because the H1N1 late-2009 season flu
virus is now the prevalent flu virus in circulation in the North
American population and for unexplained reasons the seasonal flu
threat has ceased to exist, at least at the date of writing this
report (Sept. 24, 2009). The seasonal flu has vanished this year.
Here
are the facts surrounding an investigation into the origins of
the H1N1 swine flu of 2009 as Professor Gibbs and Dr. Downie present
them, along with cited references to other important facts I uncovered
in my own investigation:
The
swine flu virus of 2009 appeared suddenly and without warning,
and evaded all routine flu surveillance and quarantine.
This
flu is not like other flu viruses seen in the past. It is
a triple-reassortant flu virus.
Examination
of the longer phylogenetic branch length compared to its nearest
genetic neighbors indicates that the appearance of this novel
H1N1 swine flu virus of 2009 is unlikely to be a recent event.
[Virus Genes, early online, August 20, 2009] But this
would mean it had to be in circulation for many years, for
which there is no evidence. However, a long development period
assumes natural variation and gene mutation rates, not mutations
induced by artificial means, or the actual creation of this
virus in a laboratory and subsequent instillation into human
populations.
Six
of this flu virus’ genes came from a "triple-reassortant"
influenza virus (or viruses).
These
viruses were found in North American pigs more than a decade
ago, then completely disappeared, and have never been found
in Europe. The other two genes came from Eurasian "avian-like"
viruses common in Europe for longer, but never found in North
America. However, both groups of H1N1 viruses have been found
recently in pigs in southeast Asia.
Movement
of live pigs between Eurasia and North America may have facilitated
mixing of diverse swine influenzas, leading to the multiple
reassortant events. This goes unquestioned. But there is a
strong reason to think the possibility of swine-to-human transmission
is a misdirection.
While
pigs are exported from one country to another, they are exported
from North America to Asia, not the other way around.
Strict
quarantine measures are employed when pigs are exported so
as not to contaminate an existing herd with disease. Usually
imported pigs are kept in quarantine, away from a larger herd,
for a period of two weeks. If an imported herd brought a suspect
gene sequence with it, it would have had to somehow evade
quarantine measures.
The
development of this virus would require at least two trans-continental
trips to get together in one place, and hence this theory
requires at least two quarantine failures, probably three
say Drs. Gibbs and Downie. This is not likely.
None
of the genes found in this swine influenza had been in current
circulation. The NA (nearuaminidase) gene had not been identified
in samples for 17 years before it reappeared in early 2009,
and the others, including the MP gene, for around 11 years.
Drs. Gibbs and Downie say this suggests the virus emanated
from a swine herd vaccine. Or it could have emanated from
an accidental release from an infected human working at a
vaccine plant, or it was intentionally induced into human
populations in Mexico.
If
this virus had originated earlier then most likely it would have
spread to the human and/or pig populations earlier, and would
probably have been detected as there are hundreds of influenza
monitoring stations across the globe.
Laboratories
house a range of flu viruses which could explain why the swine
flu of 2009 escaped detection for years and reappeared. Such a
laboratory escape would not require generations to produce mutations
or variations and reassortants.
Labs
that develop and combine viruses in multivalent swine herd
vaccines are a likely source of recombination. This avenue
of investigation has not been adequately pursued. But again,
there is strong reason to believe contaminated animal vaccines
are not involved here.
According
to Drs. Gibbs and Downie, the simplest scenario is that a
contaminated multivalent vaccine was not fully sterilized.
There
has been no report of an outbreak of a H1N1 swine flu virus
in a pig herd in the USA, whereas it has been reported among
unvaccinated pig herds in other parts of the world; two each
in Canada and Australia, and one in Argentina. This would
suggest animal vaccination may have something to do with the
origins triple reassortant flu viruses. But again, strong
skepticism of this idea should be expressed.
Historically,
influenza was not first recognized clinically in pigs until
the late summer and fall of 1918 in the midwestern United
States. This gives rise to the notion that the Spanish flu
of 1918 was spread to swine herds from humans. This is why
this year’s late-season flu outbreak has health officials
worried. Is this a re-play of the deadly 1918 Spanish flu
pandemic?
The
H1N1 influenza lineage that circulated in the human population
for four decades after the 1918 Spanish influenza epidemic,
disappeared during the 1957 Asian influenza pandemic and reappeared
in 1977. Drs. Gibbs and Downie note that the H1N1 that reappeared
was found to be genetically close to an H1N1 isolate collected
in 1950, indicating that it had probably been held in a laboratory
freezer between 1950 and 1977.
Drs.
Gibbs and Downie recommend immediate action to:
Obtain
samples of all flu variants used in swine herd vaccines in North
America.
Identify
stocks of refrigerated swine viruses which should be checked
for gene sequencing.
Examine
quarantine measures when swine herds are moved from one part
of the world to another to determine if quarantine measures
are adequate.
But
these efforts may prove to be fruitless in determining the origin
of this flu outbreak.
Since
1997, novel viruses of three different subtypes and five different
genotypes have emerged as agents of influenza among pigs in
North America. The appearance of these viruses is remarkable
because there were no substantial changes in the overall epidemiology
of swine influenza in the United States and Canada for over
60 years prior to this time. Viruses of the classical H1N1 lineage
were virtually the exclusive cause of swine influenza only from
the time of their initial isolation in 1930 through 1998. [Virus
Research 2002 May 10;85(2):199210]
Since
1998 triple reassortant swine influenza viruses have been isolated
from pigs in the United States and a human case of a triple
reassortant swine flu infection was reported in the US as early
as 2005. This patient was exposed to freshly-killed pigs. [Emerging
Infectious Diseases 2008 Sep; 14(9):14702]
A report
published in The New England Journal of Medicine in June
of 2009 indicates triple-reassortant swine flu influenza A H1
viral infections were reported among a few humans who worked
closely with pigs from 2005 to 2009. [New England J Medicine.
2009 Jun 18; 360(25):261625] However, this is not the
exact flu virus that is currently sweeping globe with a late
season onset in 2009.
Michael
Gregor MD claims crowding in pig farms is a factor in the development
of the current triple reassortant flu virus infecting humans,
asserting its precursor was first discovered in pig herds in
North Carolina in 1998. North Carolina is the home of the nation’s
largest pig farms. And it’s true, 3/4ths of the genetic material
in the H1N1 human swine flu of 2009 comes from this 1998 pool
of swine viruses. [Humane Society, August 26, 2009] But again,
this may be a misdirection.
Sometimes
the obvious is not recognized. With all of the prior discussion
about swine-origin influenza, this H1N1 late-2009 flu season
virus is not currently found in pig herds, says Vincent Racaniello
PhD, Professor of Microbiology at Columbia University Medical
Center. The virus may have originated in a human! Asking the
question "where did ‘pig zero’ come from?" may be
the wrong question. Wikipedia accurately acknowledges that "the
2009 H1N1 virus is not zoonotic swine flu (zoonotic = transmitted
from animals to people), as it is not transmitted from pigs
to humans, but from person to person."
The tracking
of the lineage of this virus has been perplexing if for no other
reason than the misdirection to investigate herds of pigs. News
reporters may have been misled from the outset. For example,
Karen Kaplan of The Tribune Newspaper wrote on Sept.
13, 2009 that "Somehow, a single pig became simultaneously
infected with that virus and a pure swine flu strain found in
pigs in Europe and Asia. The two strains swapped genetic material
to produce the new H1N1 strain, which then began to infect humans."
But the virus has not been detected in swine herds so far. It
is similar to other reassortant flu viruses, but not the same.
The current
H1N1 outbreak in Mexico in early 2009 was predicted by Replikins,
a Boston-based biotech company in April of 2008 using human,
not pig data. Replikins also indicates it alerted public health
authorities and government agencies of its prediction. Replikins
says changes in Replikin Count have been shown to precede the
clinical reality by six to 12 months in all other influenza
outbreaks of record. The company says it has demonstrated that
all influenza pandemics and epidemics, and their cessation,
over the last 90 years have been associated with statistically
significant changes in the concentration (Replikin Count)
of a particular group of genomic peptides of the virus associated
with rapid replication (Replikins). Was government tipped off
ahead of time over the appearance of this triple reassortant
flu virus?
Replikins
bases their predictions upon analysis of something called the
"Replikin Count" or number of Replikins
per 100 amino acids. The company claims, in all three of the
last century’s influenza pandemics (H1N1 in 1918; H2N2 in 1957;
and H3N2 in 1968) the amino acid sequences of the reported strains
exhibited a strain-specific increase in the Replikin Count
peptide quantities.
Replikins
also claims the Replikin Count reached 7 – the same level
achieved during the H1N1 1918 Pandemic. However, this dreaded
H1N1 late-season flu outbreak of 2009 has not produced a significant
increase in mortality to even approach the mortality rate of
the 1918 Spanish Flu. About 1020% of those who were infected
with the Spanish Flu of 1918 died. [Wikipedia] The
fatality rate for the late-season 2009 flu outbreak is estimated
at 0.5%, or 5 deaths per 1000 people infected.
Replikins
also claims at its website that "This month (July 2009),
Replikins, Ltd. was contacted by and reached out to senior government
health officials in dozens of countries to offer the FluForecast®
service. Many countries plan to introduce the service to their
public health surveillance programs both for early warning and
for tracking epidemics." But the Replikins system did not
accurately predict severity. Did the Replikins predictive technology
mislead governments throughout the world, who had foreknowledge
of the flu outbreak in Mexico, of its severity?
The origin
of the late-2009 seasons H1N1 flu virus, or "patient one"
may be a person in Mexico or elsewhere who was given a multivalent
seasonal flu vaccine and/or anti-viral drugs (i.e. Tamiflu)
and in whom mutations occurred. But even then, this does not
explain the wide and near-impossible gene segments that originated
from different continents and would have had to reassort more
than twice.
If a pig
was not the origin of the novel H1N1 late season flu virus of
2009 then did this influenza reassort in a human? Investigative
journalist Wayne Madsen, using an unnamed virologist as the
source of his information, is the only journalist that I can
find to claim the late-season triple reassortant flu virus of
2009 emanated from a laboratory strain that was implanted into
a human, who served as a "guinea pig" to permit the
exchange of genes seen in this virus. All that is known is that
the first late-2009 season H1N1 flu virus occurred in a human
and that it is not a "swine virus" but a "human
virus." Madsen’s unnamed expert virologist also says, contrary
to many news reports, there is no evidence that RNA/DNA from
the 1918 influenza virus has been detected in this 2009 H1N1
strain. Madsen’s virologist throws up his hands to explain the
exact origin of this pandemic H1N1 flu virus of 2009 by saying
"technology can create any kind of virus you want."
[Wayne Madsen Reports Sept. 16, 2009]
Fear of
a mutated flu virus which no one has antibodies towards is the
great fear of all public health officials.
Over-reliance
upon vaccination and anti-flu drugs increases genetic pressure
for flu viruses to mutate into treatment-resistant forms. Genetic
mutation is accelerated with the use of vaccines and antivirals.
[PLoS One 4(3):e4915, March 18, 2009; Virology Journal 5: 13339,
October 2008]
Just how
do flu viruses mutate within a human? It is known that bursts
of free radicals can induce gene mutations in viruses. [FASEB
Journal 2000 Jul; 14(10):144754] Vaccination of birds
and humans against the flu has been shown to apply genetic pressure
and induce more rapid genetic drifts. [Virology Journal 2008;
5: 15]
Bursts
of free radicals emanate from what is called a "cytokine
storm." Cytokines are substances that are secreted by specific
cells of the immune system and can increase 1000-fold during
infection. Over-reactive cytokine response is attributed to
the fatality rate of flu viruses. [Mikrobiyol Bulletin 2008
Apr;42(2):36580]
Whole
inactivated or so-called "killed" viral vaccines,
which are the most commonly used, are plagued by their inability
to activate antibodies. So they generally require strong adjuvants
and several injections to be fully effective. [Clinical Microbiology
Review 2007; 20: 489510] Adjuvants are pharmacological
or immunological agents that modify the effect of other agents
(e.g., drugs, vaccines).
MF59,
the favored squalene-based adjuvant employed in both swine herd
and human vaccines, could possibly trigger mutations that make
flu viruses treatment resistant. Researchers indicate MF59 does
indeed induce greater immune response due to its ability
to generate cytokines! [Proceedings National Academy Sciences
U S A. 2008 Jul 29; 105(30):105016]
It has
been repeatedly shown that nutritional deficiencies, particularly
of vitamin E and the trace mineral selenium, exacerbate the
immune response to replicating flu viruses and that this then
leads to alterations in the gene makeup of the viral genome,
resulting in a mortal outcome. [Trends Microbiology 2004 Sep;12(9):41723]
Nutritional deficiency not only affects the host response to
the virus but also the viral genome itself. [Proceedings Nutrition
Society 1999 Aug;58(3):70711] To limit mortality, public
health officials should be fortifying foods with selenium and
vitamin E to head off the possibility of gene mutations among
flu sufferers. [J Trace Element Med Biol. 2007;21(1):5262]
It’s
obvious that public health officials are more intent upon preparing
a vaccine to address an impending flu outbreak late this fall in
North America than asking where this H1N1 swine-origin triple-assortment
influenza virus came from and how it developed.
The
low mortality rate associated with this flu outbreak does not deserve
the attention the news media has given it or the widespread preparations
that public health authorities have made.
The
$9 billion the U.S. allotted to fight a flu that has crossed continents,
that did not spark a deadly flu outbreak in South America during
their flu season, and which so far has resulted in fewer deaths
than recent past seasonal flu outbreaks in North America, speaks
for intentional misdirection or even possible conspiracy involving
vaccine makers and politicians to create a flu pandemic.
That
the so-called swine flu was first observed in Mexico just at the
same time Nicholas Sarkozy, president of France, was visiting there
to announcement the establishment of a new French vaccine plant
in Mexico, has to be more than coincidence.
It
is obvious, cash-strapped local health authorities want the money
being offered by the federal government and are being bribed into
stirring up flu hysteria. According to the latest survey, about
49% of Americans are ready and willing to be vaccinated for this
unusual flu strain that struck North America late in the 200809
flu season, in an alleged pattern similar to the deadly flu pandemic
of 1918.
It
appears governments around the world had foreknowledge of this viral
pandemic. Not only did Replikins, a Boston-based biotech company,
warn governments in 2008 of developing flu viruses that were of
concern, but The Federal Emergency Management Agency (FEMA) began
drills to administer vaccines in South Texas prior to the first
cases this flu in Mexico beginning March 18, 2009. FEMA
began pandemic flu preparations as early as 2007. The
US Treasury Department also began coordinated flu pandemic preparations
with Homeland Security also in 2007.