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From: TSS ()
Date: June 29, 2005 at 3:04 pm PST


##################### Bovine Spongiform Encephalopathy #####################

part 2;

page 10 of 10

cattle under 30 months of age present no risk of harboring BSE prions and
thus, cannot cause vCJD in humans.

22. Prion diseases are invariably fatal and no vaccine, antidote or cure
exists to treat them. Similar to the human prion disease, it is likely that
the spontaneous (or sporadic) for of BSE accounts for many cases in cattle
and thus prions will not disappear from livestock simply by eliminating
prion-infected feeds. That being the case, it is imperative for the USDA to
implement measures that address this public health thread and mitigate the
risk of transmission as much as possible which should include the testing of
all cattle slaughtered in the United States.

I declare under penalty of perjury under the laws of the United States of
America that the foregoing is true and correct. Executed on June 28, 2005

Stanely B. Prusiner, M.D.


NO wonder my PDF reader would not read the rest of Stans testimony, just
more BSe about spontaneous BSE/TSE with absolutely no proof what so every
that many cases of any TSE arises spontaneously. PDF reader did not believe
it either. but would be a handy tool to sell more rapid tests. i cannot
believe i said that, but there is absolutely no science to support stans'
claim that ;

>Similar to the human prion disease, it is likely that the spontaneous (or
sporadic) for of BSE accounts for many cases in cattle...<

IF the incubation times, the neuropathological lesion profiles, and the
Gdn1/2 values indicate that MoSP1 test tube prions differ from RML and many
other prion strains derived from sheep with scrapie and cattle with bovine
spongiform encephalopathy, then what proof does Stan have that in deed ;

>Similar to the human prion disease, it is likely that the spontaneous (or
sporadic) for of BSE accounts for many cases in cattle...<

Conclusions and perspectives
The nature of the infectious agent associated with TSE has been one of the
most heated debates in the biological sciences. The evidence in favor of the
heretical protein-only hypothesis is extensive and is transforming the prion
concept into a new dogma with vast implications for diverse areas of
biology. Prions, defined as infectious proteins with the ability to transmit
biological information through the propagation of alternative protein
folding, represent an entirely new mechanism for expanding phenotypic
diversity without changes in the genome2, 51. Skeptics argue, however, that
the prion hypothesis is still not definitively proven32, 38. It is widely
agreed that the final proof of the protein-only hypothesis will require the
engineering in vitro of a synthetic infectious protein capable of
propagating a prion in vivo. These experiments have now been completed
successfully using the yeast prion Sup35 protein54, 55, coming tantalizingly
close to be the long-awaited definitive proof of the prion hypothesis. But
do these studies demonstrate that prions are the infectious agents
associated with TSEs? No—they demonstrate that the biological principle
underlying prions is correct and that the nature of the strain phenomenon
indeed resides in the propagation of alternative protein folding. However,
the challenge of transmitting disease for an infectious agent composed only
of a protein is greater in a multicellular organism than in yeast. The
protein must resist biological clearance mechanisms, get to the right place
in the brain, be propagated from cell to cell and induce specific cerebral
damage that is different depending on the exact folding of the infectious
agent. Until successful generation of infectivity by in vitro production or
amplification of PrPres can be demonstrated, it remains possible that
misfolded PrP is not the only component of the prion infectious agent.

4:15 Disease Phenotype and Transmission Properties of Bovine Amyloidotic
Spongiform Encephalopathy
Dr. Gianluigi Zanusso, University of Verona, Italy
By active surveillance system on BSE, two cows of 11 and 15 years with a
previously unrecognized form of prion disease (bovine amyloidotic spongiform
encephalopathy or BASE) were recognized. Differently from typical BSE this
novel form is characterized by the presence of PrP positive plaques and
molecular PrPSc characteristics similar to those encountered in a distinct
subtype sCJD. An update on strain characterization upon transmission
experiments will be presented.

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02)

New e-mail: (active from now)



full text ;

BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic

Creutzfeldt-Jakob disease

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

show me the data...TSS

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