Double Blow

[Guest guest]

SOURCE: Science Magazine Report, 21 March 1997, Dr. Jeffrey Taubenberger et. al. See http://www.sciencemag.org/cgi/content/abstract/275/5307/179

 

 

Taubenberger’s initial report identified the 1918 killer virus as a “novel” (new) swine flu that “recombined” avian (H5N1) as well as human (H3N2) virus fragments in its RNA structure.

 

Taubenberger used a complex computer program to perfectly match the RNA and DNA structures, and then successfully replicated and “resurrected” the 1918 killer flu as a powerful biological weapon in 2003...

http://educate-yourself.org/cn/ottswinefluweapoized1918spanishflu02jun09.shtml

 

and this...

 

In 1948 Heinrich Mueller, the former head of the Gestapo, told his CIA Interrogator that the most devastating plague in human history was man-made. He was referring to the influenza pandemic of 1918-1919 that infected 20% of the world’s population and killed between 60 and 100 million people. Mueller said the flu started as a US army bacteriological warfare weapon that somehow infected US army ranks at Camp Riley KS in March 1918, and spread around the world...

 

General Walter Schreiber, Chief of the Medical Corps of the German Army told Mueller that he had spent two months in the US in 1927 conferring with his counterparts. They told him that the “so-called double blow virus” (i.e. Spanish Flu) was developed and used during the 1914 war. “But,” according to Mueller, “it got out of control and instead of killing the Germans who had surrendered by then, it turned back on you, and nearly everybody else.”

 

 

http://1914-1918.invisionzone.com/forums/index.php?showtopic=130011

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1918 RBD Polymorphsm in Ukraine H1N1?

 

 

It is looking more and more like the 1918 Spanish flu strain. This is a killer with 2-3% mortality rate. The young and the healthy died within a day of hemorrhaging lungs: “Alive and chirpy in the morning! Dead in the evening!” It was so bad every family was affected. Coffins ran out! Let’s hope for the best but prepare for the worse. This report is still pretty much intelligent assessment/guesswork. We still need DNA sequences to confirm. Recombinomics Commentary 04:22November 9, 2009 The recent explosion of H1N1 cases in Ukraine (see map) has focused attention on sequences linked to the outbreak, especially those in the lungs of patients who developed a cytokine storm. This hemorrhagic pneumonia has been described previously in other fatal swine flu infections, but that rapid increase in reported deaths in Ukraine has raised concerns that the virus is transmitting more efficiently, or is replicating at higher levels in lung tissue. These changes are frequently linked to changes in the receptor binding domain (RBD) in the HA protein. Changes in this domain can affect affinity for receptors and also modify tissue tropism. The recent expansion of seasonal H3N2 with M2 S31N was linked to two changes in or near the receptor binding domain, S193F and D225N. Recent isolates from Sao Paulo, Brazil, collected from necropsy tissue from fatal cases had two changes at position 225.. Two of the isolates, A/Sao Paulo/53845/2009 and A/Sao Paulo/53838/2009) had D225N (see list), the same change seen in seasonal H3N2. Interestingly, the swine H1N1 is a triple reassortant with flu genes from swine, humans, and birds. The human gene is PB1 and it was acquired in swine infected with a human H3N2. The initial isolates had three human genes, the H3 and N2 as well as the PB1. Thus, the prior association of the human PB1 in isolates with human H3,may increase the advantage offered by D225N. However, two other isolates from Sau Paulo, A/Sau Paulo/53225/2009 and A/Sau Paulo/53206/2009, collected from the lungs of fatal cases, had another change at position 225, D225G. This polymorphism is more widespread and recent isolates have been found in Japan, Italy, and China (see list ). Moreover this polymorphism has been found in two isolates from the 1918/1919 pandemic, A/New York/1/1918 and A/London/1/1919. Thus, in 1918 the H1N1 virus usually had a D at position 225, but some of the later isolates had D225G, which parallels the data from the 2009 swine H1N1 isolates. These RBD changes in recent isolates from Sao Paulo, as well as the presence of D225G in sequences from 1918/1919 raise concerns that the swine H1N1 is adapting to its human host by acquisition of RBD polymorphisms. The explosion of cases in Ukraine, and delays in the release of sequences from fatal cases in Ukraine is a cause for increasing concern. Recent accelerations of deaths have been widespread across the northern hemisphere, raising concerns that receptor binding domain changes described above, as well as a third polymorphism at position 225, D225E, (see list) are gaining traction as the swine H1N1 adapts to human hosts. An update on the Mill Hill sequences and deposit of such sequences at a public database such as GISAID, where Mill Hill recently deposited sequences from Europe, would be useful.

 

 

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