Saturday, September 26, 2009
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.
(ARTICLE CONTINUES BELOW)
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):199–210]
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):1470–2]
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):2616–25] 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 10–20% 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: 133–39, 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):1447–54] 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):365–80]
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: 489–510] 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):10501–6]
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):417–23] Nutritional deficiency not only affects the host response to the virus but also the viral genome itself. [Proceedings Nutrition Society 1999 Aug;58(3):707–11] 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):52–62]
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 2008–09 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.
This article was posted: Saturday, September 26, 2009 at 5:47 am