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Working in high biosecurity laboratories, those scientists are looking to see whether changing the code of modern day Yersinia strains to include those substitutions would ramp up the virulence of the bacteria. They are doing the work in chemical assays, not animals.
As required by the rules of scientific publishing, Poinar's team will put the sequence for the ancient Yersinia bacteria into Genbank, an open access database.
He acknowledges that will likely cause alarm in some quarters. "I think it makes some people nervous," he said. "(But) science has to move forward and we need to know if these are indeed changes and could these changes account for the increased virulence and can we control for that virulence today."
"It's very cool," said Dr. Jeffery Taubenberger, the American scientist who led the effort to find and sequence the virus responsible for the 1918 Spanish flu pandemic, the only previous time a pathogen of old has been decoded. To have gone from tiny fragments of DNA to the completed genome is "an extraordinary technical advance," said Taubenberger, who runs a lab at the U.S. National Institute of Allergy and Infectious Diseases in Bethesda, Md.
"Even up to a year ago it was basically a pipe dream to get this level of genomic information," he said in a telephone interview.
In devastating the population, it changed the human immune system, basically wiping out people who couldn't deal with the disease and leaving the stronger to survive, said study co-author Hendrik Poinar of McMaster University in Ontario.
People still get the disease, usually from fleas from rodents or other animals, but not that often. There are around 2,000 cases a year in the world, mostly in rural areas, with a handful of them popping up in remote parts of the United States, according to the Centers for Disease Control and Prevention.
In devastating the population, it changed the human immune system, basically wiping out people who couldn't deal with the disease and leaving the stronger to survive, said study co-author Hendrik Poinar of McMaster University in Ontario.
…..in the early 1960s, Christian Anfinsen showed that the proteins actually tie themselves: If proteins become un-folded, they fold back into proper shape of their own accord; no shaper or folder is needed. …..Anfinsens investigation of what some call the second genetic code….
….the protein-folding problem isn’t always a problem. The very same types of misfoldings that cause dreadful diseases in some circumstances can have beneficial effects in others. The protein-folding problem is as ancient as life itself; it makes sense that evolution would occasionally, perhaps even often, use it to advantage.
In devastating the population, it changed the human immune system, basically wiping out people who couldn't deal with the disease and leaving the stronger to survive, said study co-author Hendrik Poinar of McMaster University in Ontario.
People still get the disease, usually from fleas from rodents or other animals, but not that often. There are around 2,000 cases a year in the world, mostly in rural areas, with a handful of them popping up in remote parts of the United States, according to the Centers for Disease Control and Prevention.
...made me think of the eye problem known as cataracts.
I've learned that the eyes are transparent because the cells are misaligned and when cataracts happen, it is because the cells realign themselves. Could it be related to the folding and unfolding of proteins?