Connect The Prions - Dairy
And Meat Industries In
Grave Trouble
By Jeff Rense
Not only is Mad Cow/CJD found in meat, it could be in a glass of milk, slice of cheese, bowl of ice cream.
Now there is 'official' confirmation CJD is in human blood...and transmissible via that blood. Just like HIV, just like Hep C, and so many other 'emerging diseases.' Ergo, Mad Cow prions are also in the blood of infected cattle. There is little reason to think otherwise. And remember, there is no way to tell if an animal or human is infected...and infectious...until they practically drop dead. Blood is where dairy milk comes from in the udder. Therefore, one must suspect that these incredibly small proteins (prions) could easily find their way into dairy products of all types. Infected batches of milk mixed with untold thousands of gallons of uninfected milk at any dairy is all it would take...and that is exactly what happens with milk. The dairy and beef industries are probably working around the clock, planning new milk moustache and hamburger ads to assure everyone their products are completely safe. Let's watch how the media is played and manipulated to keep the public from connecting the dots. Oh yes, remember there has never been a single case of Mad Cow/CJD reported in a single cow in America...ahem. Also, keep in mind, the Mad Cow prion and the CJD prion are exactly the same...see following story below. No, pastuerization will not eradicate prions from dairy products...prions can withstand temperatures of 1,000 degrees fahrenheit. How many prions does it take to become infected? As Clint Eastwood once said: "Do you feel lucky today?"
Blood Donors Feared to Have Spread CJD
By Jonathon Leake - Science Editor 9-17-00
Blood donated by seven people who subsequently developed variant CJD, the human form of mad cow disease, may have infected transfusion products given to many more patients, it was revealed this weekend.
The National Blood Authority has confirmed that some of the blood taken from the seven was pooled - mixed with the blood or blood products of many other donors - before it was distributed to hospitals.
The number of people who may have been affected is unknown. The authority has objected to suggestions that thousands are at risk, but has no estimates of its own.
The revelations follow experiments which show that blood from sheep that are incubating BSE but have no symptoms can transmit the disease to other sheep. Humans are equally vulnerable: blood taken from anybody incubating vCJD could theoretically spread the disease to people given blood products.
Such a case has not yet been seen with blood, although dozens of people contracted a slightly different form of CJD after being given a human growth hormone that had been extracted from corpses.
Blood from donors is usually split into its components, such as red cells, which carry oxygen; plasma, with white cells that help fight infection; and platelets, which aid clotting.
This weekend the authority confirmed that it is now considering a complete ban on the use of plasma from British donors. Most plasma is already imported, but about 100,000 units come from within Britain. The possibility that recipients of transfusions have been infected may also disqualify them from becoming blood donors.
Carlene Dyas, a spokeswoman for the authority, confirmed that the blood donated by the seven vCJD victims was taken before 1999, when the authority introduced new safety procedures designed to remove prions, the infectious proteins thought to transmit vCJD. She said: "It is very worrying, but there is nothing to show that what happens in sheep does apply to humans."
Dyas said most of the blood recipients could not be traced because records were not sufficiently detailed. More than a dozen patients known to have received blood products from people who later developed vCJD have been identified, but will not be told of the danger.
The problem is reminiscent of the spread of HIV in the 1980s when blood products transmitted the Aids virus to more than 1,200 haemophiliacs. The mistake cost the government £80m in compensation payments.
Professor Peter Smith, acting chairman of the government's spongiform encephalopathy advisory committee, confirmed there was a risk: "The concern with pooled blood products is that, as with growth hormone, an infection in one person could be spread."
Smith also acknowledged that the measures taken so far to prevent donated blood infecting others may be insufficient. Since last year, all Britishdonated blood has been stripped of its white cells, which are thought most likely to carry the infectious prion particles. Recent research indicates, however, that prions may also be carried by red cells.
CJD And Mad Cow/BSE Shown To Be The SAME Infectious Protein
From The University California, San Francisco 1-5-2000
"Researchers are reporting what they say is the most compelling evidence, to date, that the infectious proteins called prions that cause bovine spongiform encephalopathy (BSE), or "mad cow" disease, have infected humans, causing fatal brain degeneration.
Recent studies have suggested that the outbreak of mad cow disease in the late 1980s in Great Britain was responsible for the emergence of a new variant of Creutzfeldt-Jakob disease, a fatal brain-degenerative disease in humans also caused by prions. However, the link has been inconclusive. The current study establishes that the particular strain of prions, responsible for mad cow disease, is, in fact, the same strain that causes new variant Creutzfeldt-Jakob disease.
The finding, reported in the December 20 issue of Proceedings of National Academy of Sciences, is particularly unsettling because it undermines the comforting presumption that a "species barrier" dramatically lessened the likelihood that people exposed to "mad cow" disease through meats, cosmetics, and medicinal supplies would be infected. The species barrier refers to the relative lack of susceptibility of one species to prions derived from another species.
While Great Britain took the necessary measures in the late 1980s to limit spread of the disease, the disease is believed to incubate for at least 10 years, making it impossible to predict, the researchers said, how many people have been infected.
More than 175,000 cattle, primarily dairy cows have died of BSE during the past decade. More than 50 teenagers and young adults have died of new-variant Creutzfeldt-Jakob disease (nvCJD) since 1995. Nine new deaths from CJD were reported in the last quarter of 1998.
While the origins of BSE remain obscure, one possibility is that the cattle developed the disease by being fed meat and bone meal contaminated with prions from the sheep with the disease, scrapie. ...
The researchers conducted their study by first creating a line of transgenic mice genetically engineered to contain genes for the bovine prion protein. (Prion proteins are not, in themselves, lethal. They exist in all mammals and birds that have been examined, including humans, and become destructive only when their shape is altered, a change that occurs either through infection by an already infectious protein or through a genetic mutation.) The line of mice was known as Tg(BOPrP).
The researchers then inoculated the mice with prions from diseased cows. And approximately 250 days after being inoculated, all of the transgenic mice developed the neurologic disease.
Next, another group of mice was inoculated with prions from the diseased mice, and this group became sick after a virtually identical period of time, confirming that the transgenic mice transmit mad cow disease prions with no detectable change of strain or species-specific properties attributable to the mice, themselves.
Finally, and most important, transgenic mice inoculated with prions from human cases of new variant Creutzfeldt-Jakob disease produced the same incubation period and pattern of brain damage as had inoculation with prions from diseased cows.
To test their findings, the researchers inoculated transgenic mice with prions from sheep with scrapie, another prion disease causing neurological damage, and determined that these prions have dramatically different biological properties.
"BSE and new variant CJD produce the identical disease pattern of disease in Tg(BOPrP) mice, and those characteristics were those different than that found with inocula from other CJD cases or scrapie from sheep. These findings argue unequivocally that BSE and new variant CJD are the same strain of prion," said senior author DeArmond.
"The fact that the human new-variant CJD prions so precisely duplicate the properties of native bovine BSE prions in their behavior on transmission to the transgenic mice creates a compelling argument for a persuasive link between BSE and nvCJD," said Michael R. Scott, PhD, UCSF associate adjunct professor in the Institute for Neurodegenerative Diseases and the lead author of the study.
Given the enormity of the affected cattle population in Great Britain, a means of assessing risk to the human population is paramount, and more sensitive methods for detection of prions are urgently needed, the researchers said. The newly developed mouse model, Tg (BoPrP), should provide a sensitive test for detecting BSE prions, they said."
Comment (webmaster): This work was presented at the International Virology Congress in Sydney, Australia in August 1999. The full text of the PNAS article became available mid-morning on Tuesday 21 Dec 99.
This is a solid paper and another nail in England's coffin. It is fairly well described by the UCSF press release. In conjunction with earlier work, this paper shows beyond any reasonable doubt that the nvCJD is the same strain of TSE as BSE. A signficant species barrier between cattle and humans is wishful thinking given this paper and earlier data.
The paper is a watershed in that influential scientists at both the Neuropathology Unit and UCSF, while not throwing caution to the winds, are now convinced that BSE is the causal agent of nvCJD and that little by way of species barrier can be expected. It is no coincidence of timing that ten new nvCJD cases were announced yesterday, the first time ante-mortem cases have been added into the total (62 in 3 countries).
The paper is already being criticized in a whisper campaign as 'alarmist and fear-mongering' -- the idea being floated (by those responsible for the epidemic) is that nothing should be revealed because the public might panic. The top scientists are saying with this paper that they no longer can support a cover-up. The hour is late: it is high time to get out of denial and instead really light a burner under the current half-baked research effort. There will not be money for research when the government can say 'Oh, it is only 62 victims so we mustn't alarm beef importing nations unduly.'
The bovine prion gene was inserted in knockout mice that were then challenged by US Suffolk scrapie, BSE, and nvCJD. The final genomic sequence is not described in the paper despite all the problems with doppel in different knockout backgrounds -- the reader is sent off on a wild goose chase in mouse strain nomenclature in older papers. The scrapie genotypes are not provided either, other than Q at 171. Was either really determined?
While it is all well and good to test nvCJD and scrapie in these mice, this is testing the species barrier from human to cow, not really the issue except possibly for animals grazing in cemetaries. Species barriers are not necessarily symmetric, as the UCSF lab well knows from studies of mouse-to-hamster compared to hamster-to-mouse.
To test cow-to-human, a met 129 human prion in transgenic mice is needed. No one will do this, though we have val 129 (these became ill from cow, suggesting valine will prove no protection at codon 129) and chimeric met 129 mouse-human data.

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