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When the first reported cases of A/H1N1 swine flu emerged in April 2009, it was widely believed that the novel influenza strain originated in Mexico. By late June, when evidence failed to materialize confirming a Mexican origin, a new theory hypothesized that A/H1N1 originated in Asia and was transported unintentionally via an unsuspecting human carrier to North America. This though, probably is not the case. Instead it is likely, though not confirmed, that A/H1N1, is a genetically engineered creation that originated in the United States, specifically in a lab in Madison, Wisconsin that had accidentally escaped through some kind of contamination.
The evidence for this scenario is compelling:
1. Prior to the A/H1N1 outbreak, The Institute for Molecular Virology (IMV) located in Bock Labs (administered by the University of Wisconsin-Madison) had been involved in a transmission capability study for vaccine production. This study involved reverse genetic engineering of a tissue specimen that had been extracted from a deceased Intuit woman who had succumbed to Spanish influenza that had killed up to 50 million people during the 1918-19 pandemic.
2. The current A/H1N1 version is a “highly unusual virus” never seen before that combines genetic material from North American human, avian, and swine flus and Eurasian swine flu.[1] Such a combination is unprecedented having never been found in pigs, birds, or people per The Associated Press, and likely improbable to have emerged naturally. When the fact that no close relatives of the current strain exist and IMV’s mission – to conduct virology research and training at a molecular level – is taken into account, creation through artificial genetic engineering offers the best explanation.
3. Retired Australian researcher Adrian Gibbs, who played a leading role in the development of Tamiflu®, a highly-effective anti-flu drug, theorized on May 12, 2009 that the new strain of A/H1N1 likely escaped from a laboratory setting because it exhibited characteristics “of having undergone ‘accelerated evolution’ such as what happens when flu viruses try to adapt to growth in eggs” during vaccine studies.[2] Although The World Health Organization (WHO) swiftly ruled out Mr. Gibbs’ theory a day later, it is implausible that sufficient research to ascertain a conclusion could be completed in only 24 hours.
4. When A/H1N1’s existence had been firmly established in the United States by May 10, 2009, Wisconsin and Illinois had nearly a third of the country’s cases. Since then Wisconsin has consistently led the nation despite its population of 5,627,967 based on July 2008 estimates versus the larger states – California, Texas, New York, Illinois and even Michigan with July 2008 populations of 36,755,666, 24,326,974, 19,490,297, 12,901,563 and 10,003,422, respectively. By June 12, 2009 when dispersion had set in, Wisconsin and Illinois still accounted for more than a quarter of U.S. cases. Demographically speaking this disproportionate caseload makes little sense. However, when Madison, WI is viewed as the point of origin, the two-State caseload provides incontrovertible evidence of the virus’ inception. When A/H1N1 likely escaped from IMV, it immediately impacted the city’s environs and nearby locales including Illinois (since a sizeable number of Wisconsinites commute to that state each day) before spreading to Mexico (likely transmitted by a U.S. national since Granja Carroll hog farms located in La Gloria where the first case of A/H1N1 is believed to have occurred, is a subsidiary of American-based Smithfield Foods), other parts of the United States and ultimately much of the rest of the world.
Centers For Disease Control (CDC) Bulletins:
5/10/2009: Wisconsin: 357 Cases (14.1% of the national caseload); Illinois: 466 Cases (18.4% of the national caseload)
6/12/2009: Wisconsin: 3008 Cases (16.8% of the national caseload); Illinois: 1983 Cases (11.1% of the national caseload)
5. To date the A/H1N1 2009 pandemic version of swine flu has not been found to be endemic in global pig stocks discounting natural mutation and initial pig to human transmission theories. Furthermore, none of the pig stocks in Wisconsin have tested positive for the novel A/H1N1 strain that currently afflicts the world.
6. Statements and actions point to prior knowledge. As early as April 25, 2009 when the new A/H1N1 strain was officially detected in only 3 states (11 cases), a top CDC official, Dr. Anne Schuchat stated, “We do not think we can contain the spread of this virus.” By April 28, 2009 Vice President Joseph Biden ruled out quarantining Mexico citing limited benefits since “the swine flu virus [had] already penetrated many states” (64 cases in 5 states). An immediate quarantine when news of the A/H1N1 outbreak in Mexico surfaced on April 23, 2009 likely was not implemented because the CDC and top U.S. government officials had already been alerted about the accidental escape from IMV and consequent unconfirmed and unreported infections. A quarantine made little sense since cases were rapidly evolving in the United States and because such a step would likely have drawn suspicion when such cases were subsequently confirmed and reported.
7. Samples of the new A/H1N1 virus were already present at the CDC prior to receipt of Mexican specimens. Per CDC virologist Ruben Donis in an interview conducted by Science Direct (published April 29, 2009) – the CDC had completed sequencing of the novel A/H1N1 strain two weeks earlier or by April 15, 2009 – three days before Mexican officials shipped swab samples to its Atlanta headquarters for testing.
Based on the compelling facts above, conclusive evidence exists that the outbreak of A/H1N1 swine flu that has led to the WHO’s first pandemic declaration in 41 years, was created synthetically and likely can be traced back to IMV’s lab in Madison, WI. As a result, the moderate risk based on A/H1N1’s characteristics and potential threat especially to a generation that has never endured a pandemic and those with pre-existing medical conditions (asthma and other respiratory disorders, diabetes, heart problems, immune deficiency disorders, and pregnancy, to name a few) whose immune systems are ill-prepared or equipped to recognize and combat the novel strain, respectively, must be taken seriously. At the writing of this article, this is not being done (e.g. The New York City Department of Health stated on its website as late as June 25, 2009 – “Most cases of influenza-like illness do not need to be tested for H1N1” even though seasonal influenza has disappeared for the summer, failure to isolate suspected emergency room cases facilitating contagion, etc.). Continued failure to do so may result in between 1 million (based on a .25% mortality rate on existing WHO estimates that up to a third of the world’s population may be infected) to 25 million or more deaths since people will be treated much further into the illness (after serious complications have developed) and/or if the virus mutates into a more lethal form resulting in a 1+% mortality rate that is already being exhibited in Argentina, a country that has just entered the winter season.
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[1] Donald G. McNeil, Jr. In New Theory, Swine Flu Started in Asia, Not Mexico. The New York Times. 24 June 2009.
[2] Who, flu experts looking into claim swine flu evolved in lab. CBCNews.ca. 12 May 2009. 24 June 2009. www.cbc.ca/health/story/2009/05/12/swine-flu-evolution.html
Additional Source
Wayne Madsen. Hybrid A/H1N1 flu tied to genetic trigger for larger, mutated version. Online Journal. 24 June 2009. 24 June 2009. onlinejournal.com/artman/publish/article_4837.shtml
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Source by William Sutherland
