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From: TSS (216-119-144-55.ipset24.wt.net)
Subject: GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE INFECTED WITH BSE
Date: November 10, 2004 at 12:30 pm PST

-------- Original Message --------
Subject: GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE INFECTED WITH BSE
Date: Wed, 10 Nov 2004 14:34:35 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


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

Ref: MRC/62/04

Under strict embargo until 19.00 British Time Thursday 11 November 2004


GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE
INFECTED WITH BSE

New research published today (19.00 hours Thursday 11th November) by a
team from the Medical Research Council (MRC) Prion Unit offers an
explanation about why only people with a particular genetic make-up have
so far developed vCJD. It also provides evidence that other types of
BSE-derived prion infection with a different pattern of symptoms might
occur in humans. The findings are published in the journal Science.

Variant CJD (vCJD) is the human disease thought to be caused by eating
food contaminated with the infectious agent, known as a prion,
responsible for the epidemic of BSE or mad cow disease in cattle. So
far, everyone known to have developed vCJD has been of a particular
genetic type  known as MM. Until now it has been a mystery why everyone
that has developed vCJD is of the MM type and one possibility is that
they are simply the first to develop the disease when infected with BSE,
and that people with the other genetic types1 (known as VV and MV)
infected with BSE prions will also develop vCJD, but some years later.

In a series of experiments spanning more than ten years, the MRC team
has been studying mice genetically modified so that they make human
prion proteins  which are used to model human susceptibility to BSE.
The team has now shown that mice with the human VV genetic type do
become infected when given BSE or vCJD prions, but manifest a different
form of the disease which looks quite different to vCJD and has a novel
prion strain type.

Remarkably, when these novel prions were used to infect mice of the MM
genetic type, the mice either developed a disease very like vCJD, or
else a pattern of disease that looks like so-called sporadic CJD  the
classical form of CJD. This form has been known about for many years,
is seen all over the world and has not hitherto been associated with
BSE. However, the new strain identified in the mice, being called type
5, has not been seen yet in people and we do not know what pattern of
disease it would cause. It could look like one of the forms of classical
or sporadic CJD or perhaps be yet another different variant form.

The work from the MRC team suggests that type 4 prions, the type
associated with vCJD, can only propagate themselves in people that make
the M form of the protein. It seems the V form of the protein just
cannot adopt the particular molecular shape that characterises type 4.

The studies in mice also suggest that if these prions were to pass from
person to person (for example by blood transfusion) then, depending on
the genetic type of the person becoming infected, at least three
different patterns of disease might result: type 2 (which is seen in
sporadic CJD); type 4 (which causes vCJD) or type 5 (which may cause a
new pattern of disease).

Professor John Collinge, Director of the MRC Prion Unit, which is based
at University College London, said: These mouse studies give us vital
clues about the behaviour of prions and how they appear to modify and
adapt depending on the genetic makeup of the individual they are infecting.

We always have to be cautious about making direct comparison to the
human condition, but our work strongly suggests that we can not assume
only those with one genetic profile are vulnerable to BSE infection.

At this stage it is not possible to say how this should alter estimates
of those likely to become ill, but our findings do suggest we should be
taking steps to draw up a more sophisticated system of categorizing the
disease so that we dont mistake BSE related infection for a version of
sporadic CJD.

ENDS

For more information call the MRC press office on 020 7 637 6011

Notes to Editors

1The human prion protein comes in two common forms, known as M and V.
Because everyone has two copies of this gene, there are three possible
genetic types: MM, MV and VV.

Paper - Human Prion protein v129 prevent expression of vCJD phenotype 
Science On line 11.11.04

Prions are rogue forms of one of the bodys own proteins  known as the
prion protein  which are misshapen. There are several different rogue
or misshapen forms that can infect humans, and these different types of
prions are known as strains. This is analogous to different strains of
other germs such flu virus causing influenza or strains of salmonella
causing different forms of food poisoning for example.

The strain of prion causing vCJD is known as type 4, types 1-3 cause the
different forms of sporadic or classical CJD. Each strain causes a
different pattern or type of disease. It is known that prion strains can
change or mutate when they pass between different animals.

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 MRCs expenditure of £430 million is invested in its 40
Institutes, Units and Centres. The remaining half goes in the form of
grant support and training awards to individuals and teams in
universities and medical schools. Web site at: http://www.mrc.ac.uk
.


Send Post-Publication Peer Review to journal:


Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


flounder@wt.net

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, TEXAS USA 77518

################# BSE-L-subscribe-request@uni-karlsruhe.de #################





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