In general, I think that beef – deer meat "is safe in the all world", because the BSE (CWD…) is not an infectious disease. Really, also according to the recent research; BSE can be "not infectious disease". Why? At first, authors in „Journal of Pathology“ (March, 2006) found that prion proteins implicated in the development of transmissible spongiform encephalopathies, such as vCJD, may be markers for disease rather than the infectious agents. So, under laboratory circumstances prion-protein can be absorbed across the gut, it also shows that this is unlikely to occur in real life (http://www3.interscience.wiley.com/cgi-bin/abstract/112568745/ABSTRACT).

And what is about the possibility of sporadic mutations- transmission of the disease gene? There is the explanation from Dr.Murphy (President of the International Committee on the Taxonomy of Viruses), he says;
„Recent research has shown that the scrapie PrP protein differs from the BSE PrP protein at only seven amino acid loci, whereas the BSE PrP protein differs from the human CJD PrP at more than 30 loci. These differences explain the concept of strains and help explain why prions from one species might jump more easily into another species than another. It is difficult to find the terms to discuss prions -- for example, can we talk about mutants when there is no DNA? What would Watson and Crick think of all this? There is a familial form of CJD, accounting for about 10% of cases. In the familial disease there is are mutations in the gene encoding the normal protein such that the protein tends to fold in the abnormal way and tends to pile up into aggregates in brain cells with lethal consequences….. The prion protein in familial cases is the same in each family member that has it, and different in all other families. Sometimes the difference is as small as one amino acid, but these differences can be used to determine the pedigree of the prion. I'm sure such analyses are being applied to the 10 cases just reported in the UK“ (http://www.accessexcellence.org/WN/NM/madcow96.html).

Other authors in „Journal Biol. Chem.“ (November, 2006) found that small amounts of detergent-insoluble PrP aggregates are present in uninfected human brains, so insoluble aggregates and protease-resistant conformers of prion protein in uninfected human brains (http://www.jbc.org/cgi/content/abstract/281/46/34848).

More recently (February, 2007); Authors in “Neuron” wrote; “Early functional impairments precede neuronal loss in prion disease…they occur before extensive PrPSc deposits accumulate…supporting the concept that they are caused by a transient neurotoxic species, distinct from aggregated PrPSc .“ (http://www.neuron.org/content/article/abstract?uid=PIIS0896627307000086). The prion protein infection from transmissible BSE is then thought to travel to the brain via peripheral nerves, perhaps with assistance from the lymphoreticular system. In 2004, a study of 13,000 appendix and tonsil samples revealed that thousands of people may be unknowingly harbouring vCJD (http://news.bbc.co.uk/2/hi/health/6334215.stm). However, recently scientists find connection between nerve cells and immune system. They have made visible an astounding number of contacts between immune and nerve cells. These include some of the most important immune cell types, such as B-lymphocytes, T-lymphocytes and dendric cells - all of which form connections to the nerves (http://www.news-medical.net/?id=21792). The new findings, offer significant insights into normal folding mechanisms as well as those that lead to abnormal amyloid fibril conversion (http://www.sciencedaily.com/releases/2007/02/070212182836.htm). Until about five or six years ago, everyone assumed that the large amyloid plaques, or neurofibrillary tangles, that were found in the brains of Alzheimer’s victims were the cause of the disease. However, recent scientific discoveries indicate that these large, insoluble aggregates might merely be markers of the disease—they do not cause the disease (http://www.sciencedaily.com/releases/2007/02/070215110558.htm).

According to the article „Should we still be worried?“ (January 10, 2007) (http://www.guardian.co.uk/g2/story/0,,1986657,00.html), there is an agreement about the „BSE no infectiosity“ – see following text from this article; „ But despite billions spent on efforts to save Britain's beef industry and protect its citizens, all the major questions remain unanswered. The origin of the disease? A mystery. The number of people infected with vCJD? A mystery. The risk that those harbouring the disease will infect others? Again, a mystery.... The politicians didn't know what to do and the scientists didn't know what to do. We didn't know where it came from, what caused it, how bad it might be. We didn't know anything…. „The danger now is not from cattle, it's from other human beings," says another expert in vCJD ….“.
This can be in connection that the story of BSE in Britain is a consequence of „intensive farming“ (metabolic disease disease and „neurotoxicity“) and belongs in the „Organic Research“ (http://organicresearcher.wordpress.com/2007/01/06/bse-an-alternative-theory/). So, I described an alternative "BSE ammonia-magnesium" theory (http://www.agriworld.nl/feedmix/headlines.asp?issue=3). See also my "opinion- article"; about the link between BSE and Alzheimer´s disease (http://www.medicalnewstoday.com/youropinions.php?opinionid=11677). This theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia (high protein intake…). These mechanisms have a strong influence on CNS, especially in ruminants and carnivora animals. My alternative "BSE ecological view" can be well documented concerning the example "Chronic Wasting Disease" (CWD) http://organicresearcher.wordpress.com/bse-the-work-of-josef-hlasny/. See also one Chapter in my website ( http://www.bse-expert.cz).