When the first reported cases of swine flu A/H1N1 emerged in April 2009, it was widely believed that the new strain of influenza 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 inadvertently 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 in a lab in Madison, Wisconsin, that accidentally escaped through some type of contamination.
The evidence for this scenario is convincing:
1. Prior to the A/H1N1 outbreak, the Institute for Molecular Virology (IMV) located at Bock Labs (managed by the University of Wisconsin-Madison) had been involved in a transmissibility study for vaccine production. This study involved the reverse genetic engineering of a tissue sample that had been taken 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, avian and swine flu and Eurasian swine flu.[1] Such a combination is unprecedented, as it has never been found in pigs, birds or people according to The Associated Press, and is unlikely to have arisen naturally. When you take into account the fact that there is no close relative to the current strain and IMV’s mission (to conduct research and training in virology at the molecular level), 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-influenza drug, theorized on May 12, 2009 that the new A/H1N1 strain 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) quickly dismissed Mr. Gibbs’s theory a day later, it is unlikely that enough research to determine a conclusion could be completed in just 24 hours.
4. When the existence of A/H1N1 was firmly established in the United States on May 10, 2009, Wisconsin and Illinois had almost a third of the country’s cases. Since then, Wisconsin has consistently led the nation despite its population of 5,627,967 according to July 2008 estimates versus the largest states: California, Texas, New York, Illinois, and even Michigan, with July 2008 populations. 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 cases in the US Demographically speaking, this disproportionate number of cases makes little sense. However, when considering Madison, WI, 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 the outskirts of the city and nearby locations, including Illinois (since a significant number of Wisconsinites commute to that state) before spreading to Mexico (probably transmitted by a US citizen from Granja Carroll hog farms 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 United States 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 caseload); Illinois: Cases from 1983 (11.1% of national caseload)
5. To date, the 2009 A/H1N1 pandemic version of swine flu has not been found to be endemic in pig populations around the world, 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 affecting 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 just 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] 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 high-ranking US government officials The US had already been alerted to the A quarantine made little sense as cases were rapidly evolving in the US and because such a step would likely have raised suspicions when such cases were later confirmed and reported.
7. The samples of the new A/H1N1 virus were already present at the CDC before receiving the Mexican samples. According to CDC virologist Ruben Donis in an interview by Science Direct (published April 29, 2009), the 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 its 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 declaration of a pandemic in 41 years was synthetically engineered and probably traced back to IMV’s laboratory 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. At the time of this writing, this is not being done (e.g., the New York City Department of Health stated on its website on June 25, 2009: “Most cases of disease-like illnesses influenza do not need screening tests for H1N1”. despite the fact that seasonal flu has disappeared for the summer, lack of isolation of suspected cases in the emergency room that facilitates contagion, etc.). If you continue to fail to do so, it could result in between 1 million (based on a mortality rate of 0.25% 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 receive a 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 being exhibited 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, investigating 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 influenza A/H1N1 linked to genetic trigger for larger mutated version. Online magazine. June 24, 2009. June 24, 2009. onlinejournal.com/artman/publish/article_4837.shtml