The CDC, WHO and governments are saying a mutated swine flu resistant to Tamiflu results have been detected in Norway, North Carolina, U.S., Brazil, Japan, Mexico, Ukraine and the U.K.
There are many articles about this today. I am going to insert the links to them.
Here is what Wikipedia says about the 1918 Spanish flu:
Scientists have used tissue samples from frozen victims to reproduce the virus for study. Given the strain's extreme virulence there has been controversy regarding the wisdom of such research. Among the conclusions of this research is that the virus kills via a cytokine storm (overreaction of the body's immune system) which explains its unusually severe nature and the concentrated age profile of its victims. The strong immune systems of young adults ravaged the body, whereas the weaker immune systems of children and middle-aged adults caused fewer deaths.
The second wave of the 1918 pandemic was much deadlier than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. But in August, when the second wave began in France, Sierra Leone and the United States, the virus had mutated to a much deadlier form. This has been attributed to the circumstances of the First World War. In civilian life evolutionary pressures favour a mild strain: those who get really sick stay home, and those mildly ill continue with their lives, go to work and go shopping, preferentially spreading the mild strain. In the trenches the evolutionary pressures were reversed: soldiers with a mild strain remained where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. So the second wave began and flu quickly spread around the world again. It was the same flu, in that most of those who recovered from first-wave infections were immune, but it was now far more deadly, and the most vulnerable people were those who were like the soldiers in the trenches—young, otherwise healthy adults. Consequently, during modern pandemics, health officials pay attention when the virus reaches places with social upheaval, looking for deadlier strains of the virus.
One theory is that the virus strain originated at Fort Riley, Kansas, by two genetic mechanisms – genetic drift and antigenic shift – in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley to different places around the world, where they spread the disease. However, evidence from a recent reconstruction of the virus suggests that it jumped directly from birds to humans, without traveling through swine. This suggestion is slightly controversial, and other research suggests that the strain originated in a mammalian species.
An effort to recreate the 1918 flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, Southeast Poultry Research Laboratory and Mount Sinai School of Medicine in New York City; the effort resulted in the announcement (on October 5, 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from a female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers.
On January 18, 2007, Kobasa et al. reported that monkeys (Macaca fascicularis) infected with the recreated strain exhibited classic symptoms of the 1918 pandemic and died from a cytokine storm—an overreaction of the immune system. This may explain why the 1918 flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.
On September 16, 2008, the body of Yorkshireman Sir Mark Sykes was exhumed to study the RNA of the Spanish flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hope will have helped preserve the virus.
In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from 1918 flu samples to the ability of the flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing.
The original date of appearance of this virus is not clear. An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913. This ancestor virus diverged about 1913–1915 into two clades which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, it is likely that they were the original recipient of the virus. This in turn suggests that the virus was introduced into humans sometime between 1913 and 1918.
A 2005 National Geographic Article about How the 1918 Virus was dug up and the U.S. government was reproducing it to "study it".
The purpose was to get at questions relating to the 1918 pandemic," said Jeffery Taubenberger, of the Armed Forces Institute of Pathology (AFIP) in Rockville, Maryland. Taubenberger co-authored one of several related papers in this week's issues of the journals Nature and Science.
"How did this particular virus form and get into humans? How did a pandemic start?" Taubenberger said. "Why was this particular virus so virulent? And in a broader sense what can we learn from the lessons of 1918 that can help us in the future?"
Influenza viruses were unknown in 1918, so there was no way for doctors or scientists to directly study the flu during or after the outbreak.
But some institutions, like the AFIP, preserved tissue samples from 1918 flu victims. Those 87-year-old samples—and others from a victim who was buried in, and preserved by, Alaskan permafrost—yielded tiny fragments of genetic material that were used to piece together the virus's genetic coding signature.
The final genes of the virus's genome sequence are being published this week. Scientists used the completed, full viral sequence to create a live virus with the eight viral genes of the Spanish flu, named for an early, devastating outbreak in Spain.
Even if somehow released, that virus would be unlikely to cause a pandemic like that of 1918, because humans have likely acquired some immunity in the intervening decades. Nonetheless, it is currently contained at Atlanta, Georgia's Centers for Disease Control and Prevention (CDC) under extremely strict security.
I want to make sure People also KNOW - A GROUP OF PEOPLE WHO NEVER GOT THE SPANISH FLU DURING THAT TIME - WERE PEOPLE WHO WORKED IN CINNAMON FACTORIES!!
Please put Cinnamon on your List of "Must Get Items" - along with Vitamins C, D, Garlic and Kombucha Tea.
Some news out today about this "Mutated Swine Flu"
The department has examined the genetic sequence of human swine flu viruses in its monitoring system. Out of the 123 sequences studied, one sample showed the same mutation as the Norway strain.
The virus was taken from a year-old boy who developed flu-like symptoms July 22. He was admitted to Prince of Wales Hospital July 25 and discharged three days later. He has recovered.
Mutations are frequently encountered in influenza viruses. According to the World Health Organisation the same mutation of the virus has been found on the Mainland and in other countries, including Brazil, Japan, Mexico, Ukraine and the US.
The virus with this mutation remained sensitive to antiviral drugs, Tamiflu and Relenza. No evidence suggests these mutations are leading to an unusual increase in the number of human swine flu infections or a greater number of severe or fatal cases.
Portion of Article:
ATLANTA — Four North Carolina patients at a single hospital tested positive for a type of swine flu that is resistant to Tamiflu, health officials said Friday.
The cases reported at Duke University Medical Center over six weeks make up the biggest cluster seen so far in the U.S.
Tamiflu -- made by Switzerland's Roche Group -- is one of two flu medicines that help against swine flu, and health officials have been closely watching for signs that the virus is mutating, making the drugs ineffective.
More than 50 resistant cases have been reported in the world since April, including 21 in the U.S. Almost all in the U.S. were isolated, said officials with the U.S. Centers for Disease Control and Prevention.
The BBC reported another cluster of five Tamiflu-resistant cases this week in Wales, in the United Kingdom.
The CDC has sent three disease investigators to North Carolina to help in the investigation there, said Dave Daigle, a CDC spokesman. CDC testing confirmed the Tamiflu-resistant cases.
All links are embedded in their headlines.
As I see it, we have various viruses around the world being spread now. Amazing how this has come at the same time as a Global Meltdown of the Economy!
Read/Research about all the various missing lab samples from military installations, about all the microbiologist that have died over the last few years about all the discrepancies in Big Pharma vaccine information.
After doing research of how many viruses have been detected in the Swine Flu in the beginning - and now the Mutated Virus make your own mind up if all of this "Just happens to have shown up on it's own and if the Virus happened to Mutate on it's own"!
Oh, when will the WHO, CDC and Governments come out and say the "VACCINE IS WORTHLESS NOW" Since the flu has mutated and the Vaccine was NOT created for this "Mutated Strain"?