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From: TSS (216-119-144-34.ipset24.wt.net)
Subject: U.S. presents 'final' beef plan to Japan, but plan still defies BSE/TSE science and risk human health
Date: September 19, 2004 at 6:34 am PST

-------- Original Message --------
Subject: U.S. presents 'final' beef plan to Japan, but plan still defies BSE/TSE science and risk human health
Date: Sat, 18 Sep 2004 21:11:50 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


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

U.S. presents 'final' beef plan

Yomiuri Shimbun

The United States has submitted a plan under which Japan would resume
imports of U.S. beef from cows 20 months old or younger after
determining that the beef for shipment belonged to that age bracket by
examining the quality of the meat, it has been learned.

The Japanese government, which has been considering exempting beef from
cattle aged 20 months or younger from tests for bovine spongiform
encephalopathy, will not accept the U.S. proposal, insisting that it is
unscientific, officials said.

Washington aims to prepare the ground for the resumption of beef exports
to Japan at the meeting between Prime Minister Junichiro Koizumi and
U.S. President George W. Bush scheduled for Tuesday.

But as the government is disinclined to compromise on the issue, an
early resumption of imports of U.S. beef is seen unlikely.

The Bush administration, aiming to win the support of the livestock
industry ahead of the presidential election in November, is set to urge
at the Japan-U.S. meeting that Japan permit the resumption of U.S. beef
exports to Japan. The U.S. government also has hinted that it will bring
the case to the World Trade Organization if an agreement is not reached
soon.

The United States presented the plan as its final compromise offer at an
unofficial meeting with Japanese government officials held in the United
States, sources said. It proposed that beef exported to be Japan be
confirmed as coming from cattle 20 months old or younger through checks
of bone density, flesh maturity and other criteria.

The United States categorizes beef quality in five levels and would
utilize that system to check the condition of beef exported to Japan.

But the Health, Labor and Welfare Ministry and the Agriculture, Forestry
and Fisheries Ministry refuses to allow imports of U.S. beef other than
that verified as coming from cattle aged 20 months or younger, which is
the standard the Japanese government also is set to apply in exempting
cattle from domestic BSE testing on the ground that it is difficult to
detect the disease in cattle in that age bracket using the current
testing method. The ban on U.S. beef imports was imposed in December.

The government asked the U.S. government to introduce a system to record
the birth date of beef cattle. But officials said the United States is
reluctant to do so because it does not want to place a financial burden
on livestock farmers, who have significant political clout, with an
election in the offing.

On the face of it, the new proposal of the United States, which had
expressed its wish to export beef from cattle aged 24 months or younger,
looks like a climbdown on Washington's part. But Tokyo considers it
impossible that the U.S. plan would enable the age of cattle slaughtered
for beef to be confirmed accurately and thus ensure the safety of the beef.

http://www.yomiuri.co.jp/newse/20040919wo41.htm


Neurobiology of Disease
Subclinical Bovine Spongiform Encephalopathy Infection in Transgenic
Mice Expressing Porcine Prion Protein

Joaquín Castilla,1 Alfonso Gutiérrez-Adán,2 Alejandro Brun,1 Deirdre
Doyle,3 Belén Pintado,2 Miguel A. Ramírez,2 Francisco J. Salguero,1
Beatriz Parra,1 Fayna Díaz San Segundo,1 José M. Sánchez-Vizcaíno,1 Mark
Rogers,3 and Juan M. Torres1

1Centro de Investigación en Sanidad Animal, Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, Valdeolmos, 28130
Madrid, Spain, 2Departamento de Reproducción Animal y Conservación de
Recursos Zoogenéticos, 28040 Madrid, Spain, and 3Department of Zoology
and Conway Institute for Biomolecular and Biomedical Research,
University College Dublin, Belfield, Dublin 4, Ireland

The bovine-porcine species barrier to bovine spongiform encephalopathy
(BSE) infection was explored by generating transgenic mouse lines
expressing the porcine prion protein (PrP) gene. All of the porcine
transgenic (poTg) mice showed clinical signs of BSE after intracerebral
inoculation with a high-titer BSE inoculum. The protease-resistant PrP
(PrPres) was detected in 14% (3 of 22) of the BSE-infected poTg mice by
immunohistochemical or immunoblot analysis. Despite being able to infect
42% (5 of 12) of control mice, a low-dose BSE inoculum failed to
penetrate the species barrier in our poTg mouse model. The findings of
these infectivity studies suggest that there is a strong species barrier
between cows and pigs. However, after second-passage infection of poTg
mice using brain homogenates of BSE-inoculated mice scoring negative for
the incoming prion protein as inoculum, it was possible to detect the
presence of the infectious agent. Thus, porcine-adapted BSE inocula were
efficient at infecting poTg mice, giving rise to an incubation period
substantially reduced from 300 to 177 d after inoculation and to the
presence of PrPres in 100% (21 of 21) of the mice. We were therefore
able to conclude that initial exposure to the bovine prion may lead to
subclinical infection such that brain homogenates from poTg mice
classified as uninfected on the basis of the absence of PrPres are
infectious when used to reinoculate poTg mice. Collectively, our
findings suggest that these poTg mice could be used as a sensitive
bioassay model for prion detection in pigs.

Key words: BSE transmission; porcine prion; PrP; scrapie; transgenic
mice; species barrier

------------------------------------------------------------------------
Received Dec 7, 2003; revised April 7, 2004; accepted April 9, 2004.

http://www.jneurosci.org/cgi/content/abstract/24/21/5063?ct

MRC-43-00 [ ] [Text only version of this site] [Print this page]
Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
?sub-clinical? form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the ?species
barrier? - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a ?sub-clinical? form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary?s Hospital. He is also a member of the UK Government?s
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC?s expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council

http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm

UK Strategy for Research and
Development on Human and Animal
Health Aspects of Transmissible
Spongiform Encephalopathies

2004-2007

snip...

2.12.2 One of the favoured experimental models of an extreme species
barrier has been
the inability to produce clinical signs of TSE disease in mice following
infection with the
263K or Sc237 strains of hamster scrapie, and it had been assumed by
many that this
represented a complete block to the infection of mice. However, an
absence of clinical
signs does not necessarily mean that the infectious agent has not
replicated and spread
within the host, even causing recognisable lesions within the brain. For
example,
transmission of six different sources of sporadic CJD to four strains of
mice produced no
clinical signs of disease and no significant differences in survival
relative to uninfected
controls, but did result in characteristic TSE-related brain pathology
in the majority of such
mice surviving beyond 500 days224.

2.12.3 The hamster/mouse species barrier and the nature of the resultant
carrier state
have recently been revisited225-227. As expected, transmission of
hamster scrapie to mice
produced no overt disease and no evidence of TSE replication for about a
year, after which
there was active replication and adaptation of new strains capable of
causing disease in
mice, with limited evidence of PrPSc accumulation except after about 600
days. During the
first pass in mice, strains retained their virulence for hamsters, but
after three or four
successive sub-passages in mice, mouse-trophic strains emerged.

2.12.4 Subclinical infection indicative of a carrier state can also be
established after within-
species transmissions. Serially diluted, orally administered, 263K
hamster scrapie resulted
in the detection of PrPSc in some healthy animals which survived to be
culled at the end of
the experiment, some 239 days after the last clinical case. However, the
small difference
between the calculated LD50 (the ?lethal? dose which results in 50
percent of the animals
dying of clinical scrapie) and the ID50 (the dose which results in 50
percent of the animals
showing some sign of infection, which includes both scrapie deaths and
PrPSc-positive
animals showing no clinical signs) indicates that the number of carrier
animals would be
unlikely to exceed greatly the number of clinical cases228.

2.12.5 The potential existence of asymptomatic infected ?carrier?
animals or humans is of
great relevance to the effectiveness of surveillance and control
programmes for BSE,
scrapie and vCJD and needs to be pursued. Lack of detectable PrPSc would
preclude
detection by current diagnostic tests and such ?carrier? animals or
humans would
represent hidden reservoirs of infectivity, implying a risk of onward
infection to others
through natural (scrapie) or iatrogenic (human) transmission.

snip...

FULL TEXT APPRX. 91 PAGES

http://www.mrc.ac.uk/pdf-uk_strategy_v5.2.pdf

all animals for human/animal consumption must be tested...

TSS

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