Originally Posted by
BigTime1
So you are saying you can show that a deer is CWD clinically positive by only testing positive in the lymph nodes. 100% cwd positive? If this is what you are trying to make us believe feel free to show that research. !00% nodes only positive!
Hmmm. No Gene he says...
The prion gene
At some point the gene that codes for the prion protein was found. Where? In the host. That is, the prion gene -- the gene for the prion protein -- is a normal host gene. When a sheep gets a prion disease (scrapie),Deer,(Chronic Wasting Disease) the animal's own gene for the prion protein codes for any new prion protein that is produced.
A direct test showing the importance of the host prion gene for the prion disease came with mice, where it is "easy" to delete a specific gene. Mice lacking the gene for the prion protein cannot be infected with prions. (The method used to make such a "knockout mouse" is discussed briefly on the BITN page Agricultural biotechnology (GM foods) and Gene therapy - Introduction.)
Finding the prion gene solves one problem in the prion mystery. The protein does not truly self-replicate. It is coded for by a gene, a normal gene -- in fact, by a host gene. Thus the feature of the prion model which most seriously challenged our common understanding of genes and proteins is no longer a problem. Attention now turns to the question of how this host protein turns "toxic", and how its toxic form can be infectious?
That little theory (from 2007) was not only NOT proven but was debunked in 2010 buddy. Nice try again. From the US national Laboratories For Health
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933051/
Excerpt from same :
Abstract
Prions are self-propagating proteinaceous infectious agents capable of transmitting disease in the absence of nucleic acids. The nature of the infectious agent in prion diseases has been at the center of passionate debate for the past 30 years. However, recent reports on the in vitro generation of prions have settled all doubts that the misfolded prion protein (PrPSc) is the key component in propagating infectivity. However, we still do not understand completely the mechanism of prion replication and whether or not other cellular factors besides PrPSc are required for infectivity. In this article, we discuss these recent reports under the context of the protein-only hypothesis and their implications.
Key words: prions, infectivity, protein-only hypothesis, protein misfolding cyclic amplification, synthetic prion
Prions, Bizarre Infectious Agents, Unique Diseases
Prions are self-propagating particles of proteinaceous origin which share the ability to transmit disease with typical infectious organisms such as viruses and bacteria, but in contrast to them, prions do not have genetic material. Prion diseases have been found in humans and other mammals, including cattle, sheep, cervids, felines and rodents. In addition to transmission by infection, the disease can have inherited and sporadic origins. In the transmissible cases, infection of the host is preceded by a variable incubation period and followed by the appearance of clinical symptoms. Prion diseases are 100% fatal and after a long pre-symptomatic period in which the agent is slowly replicating, the clinical phase is often very rapid, progressive and severe.3
Although the exact molecular nature of prions is not completely clear, it is widely accepted in the field that the prion protein (denoted PrP) in its infectious conformation (PrPSc) is the main, or perhaps only, component of the infectious agent.2,3 Having a misfolded protein as an infectious agent makes prions very unconventional. Even if some co-factors are proven to be required, the minimal infectious agent should be much less complex than a virus or any other form of conventional micro-organism. Given the heretical nature of prions, the “protein-only” hypothesis has remained controversial for decades.4,5 Recent reports demonstrating the formation of highly infectious prions completely in vitro have provided the strongest proof for the prion hypothesis and have taken the field to an entirely new position.6–9 In this article, we summarize these findings and critically discuss their contribution to understand the molecular nature of prions and their unique mechanism of propagation
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You may click the link to read more on that PROVEN testing as I have provided a link which BigTime1 seems to fail to do with ANYTHING he says. Took me a little while to find that little excerpt he put up AND EDITED severely. Nice try again, have a nice night
