Infectious Prions Can Arise Spontaneously in Normal Brain Tissue, Study Shows

The catalyst in the study was the metallic surface of simple steel wires. Previous research showed that prions bind readily to these types of surfaces and can initiate infection with remarkable efficiency. Surprisingly, according to the new research, wires coated with uninfected brain homogenate could also initiate prion disease in cell culture, which was transmissible to mice.

The findings are being published in the online edition of the journal Proceedings of the National Academy of Sciences (PNAS).

"Prion diseases such as sporadic Creutzfeldt-Jakob disease in humans or atypical bovine spongiform encephalopathy, a form of mad cow disease, occur rarely and at random," said Charles Weissmann, M.D., Ph.D., chair of Scripps Florida's Department of Infectology, who led the study with John Collinge, head of the Department of Neurodegenerative Disease at UCL Institute of Neurology. "It has been proposed that these events reflect rare, spontaneous formation of prions in brain. Our study offers experimental proof that prions can in fact originate spontaneously, and shows that this event is promoted by contact with steel surfaces."
Infectious prions, which are composed solely of protein, are classified by distinct strains, originally characterized by their incubation time and the disease they cause. These toxic prions have the ability to reproduce, despite the fact that they contain no nucleic acid genome.

Mammalian cells normally produce harmless cellular prion protein (PrPC). Following prion infection, the abnormal or misfolded prion protein (PrPSc) converts PrPC into a likeness of itself, by causing it to change its conformation or shape. The end-stage consists of large aggregates of these misfolded proteins, which cause massive tissue and cell damage.

A Highly Sensitive Test
In the new study, the scientists used the Scrapie Cell Assay, a test originally created by Weissmann that is highly sensitive to minute quantities of prions.
Using the Scrapie Cell Assay to measure infectivity of prion-coated wires, the team observed several unexpected instances of infectious prions in control groups where metal wires had been exposed only to uninfected normal mouse brain tissue. In the current study, this phenomenon was investigated in rigorous and exhaustive control experiments specifically designed to exclude prion contamination. Weissmann and his colleagues in London found that when normal prion protein is coated onto steel wires and brought into contact with cultured cells, a small but significant proportion of the coated wires cause prion infection of the cells -- and when transferred to mice, they continue to spawn the disease.

Weissmann noted that an alternative interpretation of the results is that infectious prions are naturally present in the brain at levels not detectable by conventional methods, and are normally destroyed at the same rate they are created. If that is the case, he noted, metal surfaces could be acting to concentrate the infectious prions to the extent that they became quantifiable by the team's testing methods.

The first author of the study, "Spontaneous Generation of Mammalian Prions," is Julie Edgeworth of the UCL Institute of Neurology. Other authors of the study include Nathalie Gros, Jack Alden, Susan Joiner, Jonathan D.F. Wadsworth, Jackie Linehan, Sebastian Brandner, and Graham S. Jackson, also of the UCL Institute of Neurology.

The study was supported by the U.K. Medical Research Council.




SO, problem solved ? Are we all suppose to believe that the atypical BSE strains and sporadic CJD strains, are just another happenstance of spontaneous mutation in all cases, just an old cow disease such as sporadic CJD in humans i.e. old people disease, another spontaneous mutation in all cases of sporadic CJD. SO, we are suppose to believe that out of all these atypical BSE cases popping up around the globe, NONE were caused by feed ? I don't believe that for a New York minute. I don't believe all cases of sporadic CJD are all spontaneous either. Either the UKBSEnvCJD theory was totally wrong, or this BSe that all other TSE are of a spontaneous mutation is wrong. You cannot have your cake, and eat it too.

With headlines like, Contact with steel 'linked to CJD' , or Infectious prions can suddenly erupt from normal brain tissue , or infectious prions can arise spontaneously in normal brain tissue , I decided to wait and look at the study. glad I did. nothing about this study shows that 85% to 90% of all human TSE i.e. the sporadic CJD's show they are a spontaneous generation from nothing. It does however cause confusion, of which, in my opinion, could have been resolved. I will ask the same question here, I ask Professor Stanley Prusiner, of which I never did receive an answer, I ask this same question. OF this supposedly Spontaneous generation of mammalian prions in this study, does this mean all sporadic CJD is spontaneous? does it mean half ? does in mean one third, one tenth, one hundredth, one thousandth, one millionth, just exactly what ? what does this really show ? Does this study show what many officials and industry is hoping, that it is all spontaneous mutation from nothing ? IF so, why did the authors of this study not explain this ? THERE is something terribly wrong with this prion and the UKBSEnvCJD only theory. It just does not compute, and I believe that this study raises more questions than answers. I believe that the authors of this study should have explained better whether or not this study shows that indeed all cases of sporadic CJD are of a spontaneous mutation cause, or not. They could have done a much better job of explaining what this study shows, or what it _does not_ show, and in my opinion, it damn sure does not show that all cases of sporadic CJD strains, and or atypical BSE strains arise spontaneously, a natural mutation, without any route and source of agent. But, this is what this study insinuates, and that is how it will be interpreted by industry groups and officials. I think the Authors of this study could have better interpreted that to the public, either way, either sporadic CJD is all spontaneous, or not, if not, how much is spontaneous. After 2+ decades of debating this, they owe the public this in my opinion. Stand Tall and tell us how much of this spontaneous mutation from nothing, how much of the 85% to 90% of all human TSE (well, maybe more than that IF you include the infamous sporadic FFI?) i.e. sporadic CJD, how much of this spontaneous mutation from nothing does this consist of ? 1 in a 100 cases, 1 in a thousand, 1 in a million, 1 in a billion, of sporadic CJD and sFFI cases etc. ? please tell me, or at least tell the public that this study does NOT insinuate what it does.

My reply and question to Professor Stanley Prusiner (of which he never would answer), the same question I now address to Julie A. Edgeworth, Nathalie Gros, Jack Alden, Susan Joiner, Jonathan D. F. Wadsworth, Jackie Linehan, Sebastian Brandner, Graham S. Jackson, Charles Weissmann1,2, and John Collinge1 + Author Affiliations. ...


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Tuesday, July 27, 2010

Spontaneous generation of mammalian prions

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