When the first reported cases of A/H1N1 swine flu emerged in April 2009, it was widely believed that the new influenza strain originated in Mexico. In late June, when evidence confirming a Mexican origin failed to materialize, a new theory hypothesized that A/H1N1 originated in Asia and was unwittingly transported via an unsuspecting human carrier to North America. This, however, is probably not the case. Instead, it is likely, though not confirmed, that A/H1N1 is a genetically modified creation that originated in the United States, specifically a lab in Madison, Wisconsin, that accidentally escaped through some form of contamination.
The evidence for this scenario is compelling:
1. Prior to the A/H1N1 outbreak, the Institute for Molecular Virology (IMV) located at Bock Labs (administered by the University of Wisconsin-Madison) had been involved in a transmissibility study for vaccine production. This study involved reverse genetic engineering of a tissue sample that had been removed from a deceased Intuit woman who had succumbed to the Spanish flu that had killed up to 50 million people during the 1918-19 pandemic.
2. The current version A/H1N1 is a never-before-seen “very unusual virus” that combines genetic material from North American human, bird and swine flu and Eurasian swine flu.[1] Such a combination is unprecedented, having never been found in pigs, birds or people according to The Associated Press, and it is unlikely to have arisen naturally. When taking into account the fact that there is no close relative of the current strain and IMV’s mission (to conduct research and training in virology at the molecular level), 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 probably escaped from a laboratory setting because it exhibited characteristics “of having undergone ‘accelerated evolution,’ such as what happens when influenza viruses try to adapt to growth in eggs” during vaccine studies.[2] Although the World Health Organization (WHO) quickly dismissed Mr Gibbs’s theory a day later, it is implausible that sufficient investigation could be completed to determine a conclusion in just 24 hours.
4. When the existence of A/H1N1 became firmly established in the United States on May 10, 2009, Wisconsin and Illinois had nearly one-third of the country’s cases. Since then, Wisconsin has consistently led the nation despite its population of 5,627,967 as of July 2008 estimates versus the largest 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. . As of June 12, 2009, when the spread began, Wisconsin and Illinois still accounted for more than a quarter of the cases in the US. Demographically speaking, this disproportionate number of cases makes little sense. However, when Madison, WI is considered as the point of origin, the number of cases from two states provides incontrovertible evidence of the onset of the virus. When A/H1N1 likely escaped from IMV, it immediately affected areas around the city and nearby, including Illinois (since a significant number of Wisconsinites commute to that state) before spreading to Mexico (probably transmitted by a US citizen from the pig farms Carroll Farm located in La Gloria, where the first case of A/H1N1 is believed to have occurred, is a subsidiary of US-based Smithfield Foods), other parts of the US and ultimately much of the rest of the world.
Bulletins from the Centers for Disease Control (CDC):
05/10/2009: Wisconsin: 357 Cases (14.1% of the national number of cases); Illinois: 466 Cases (18.4% of the national number of cases)
06/12/2009: Wisconsin: 3,008 cases (16.8% of the national number of cases); Illinois: 1983 Cases (11.1% of the national number of cases)
5. To date, the 2009 A/H1N1 pandemic version of swine flu has not been found to be endemic in the world’s pig populations, discounting theories of natural mutation and initial transmission from pigs to humans. Additionally, none of the pig populations in Wisconsin have tested positive for the new A/H1N1 strain currently plaguing 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 senior CDC official, Dr. Anne Schuchat, stated: “We don’t think we can contain the spread of this virus.” By April 28, 2009, Vice President Joseph Biden ruled out quarantining Mexico citing limited benefits as “the swine flu virus [had] it had already penetrated many states” (64 cases in 5 states). An immediate quarantine when news of the A/H1N1 outbreak in Mexico broke on April 23, 2009 was probably not implemented because the CDC and senior US government officials The US had already been alerted to the accidental release of IMV and consequently unconfirmed and unreported infections.A quarantine made little sense since cases were evolving rapidly in the United States and because such a step would likely have raised suspicions when such cases were subsequently confirmed and reported.
7. Samples of the novel A/H1N1 virus were already present at CDC prior to receipt of the Mexican samples. According to CDC virologist Ruben Donis in an interview conducted by Science Direct (published April 29, 2009), CDC had completed sequencing of the new A/H1N1 strain two weeks earlier or on April 15, 2009. , three days before Mexican officials sent swab samples. to their Atlanta headquarters for testing.
Based on the above compelling facts, there is conclusive evidence that the A/H1N1 swine flu outbreak that led to the first WHO pandemic declaration in 41 years was synthetically created and likely traced back to the IMV lab in Madison, WI. As a result, the moderate risk based on the characteristics and potential threat of A/H1N1, especially for a generation that has never experienced a pandemic and those with pre-existing medical conditions (asthma and other respiratory disorders, diabetes, heart problems, immunodeficiency disorders , and pregnancy, to name a few) whose immune systems are ill-prepared or equipped to recognize and combat the new strain, respectively, should be taken seriously. As of this writing, this is not being done (eg, the New York City Department of Health stated on its website on June 25, 2009: “Most cases of AIDS-like illnesses influenza do not need H1N1 detection tests.” despite the fact that the seasonal flu has disappeared for the summer, lack of isolation of suspected cases in the emergency room that facilitates contagion, etc.). If it continues not to do so, it could result in anywhere from 1 million (based on a .25% fatality rate on existing WHO estimates that up to a third of the world’s population may be infected) to 25 million or more deaths, as people will receive much longer treatment. in the disease (after serious complications have developed) and/or if the virus mutates to a more lethal form resulting in a mortality rate of more than 1% that is already on display in Argentina, a country that has just enter the winter season.
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[1] Donald G. McNeil, Jr. In a new theory, swine flu started in Asia, not Mexico. The New York Times. June 24, 2009.
[2] Who, researching flu experts claim that swine flu evolved in the laboratory. CBCNews.ca. 2009 May 12. 2009 June 24. www.cbc.ca/health/story/2009/05/12/swine-flu-evolution.html
additional source
Wayne Madsen. Hybrid A/H1N1 flu linked to genetic trigger for larger mutated version. Online magazine. June 24, 2009. Retrieved June 24, 2009. onlinejournal.com/artman/publish/article_4837.shtml