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From: TSS (
Date: November 11, 2004 at 11:28 am PST

-------- Original Message --------
Subject: Mice with 'good' genes succumb to vCJD
Date: Thu, 11 Nov 2004 13:24:12 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

Published online: 11 November 2004; | doi:10.1038/news041108-14

Mice with 'good' genes succumb to vCJD

Jim Giles

New strains of Creutzfeldt-Jakob disease may yet emerge.

Researchers fear that the right genes may not protect from the
brain-damaging effects of vCJD.


People with genes thought to protect against variant Creutzfeldt-Jakob
disease (vCJD) may still be at risk of developing some strains of the
illness, animal studies suggest.

All of the 146 British people who have died from vCJD, which is thought
to be caused by eating meat infected with the prion protein that causes
mad cow disease, have a genetic variation known as MM. This led some
researchers to hope that people with different variants, who make up 60%
of the population, may be protected from the disease.

But mice with such supposedly protective genes still seem to be
susceptible to infection with the rogue protein, report John Collinge
and colleagues at University College London in a paper published online
by Science1
Researchers are cautious about the study's implications for humans, but
say that it adds weight to the possibility that tainted beef could have
infected more people than was originally thought.

In future we might see different types of CJD.

Markus Glatzel
University of Zurich in Switzerland

"In future we might see different types of CJD," predicts Markus
Glatzel, who studies the disease at the University of Zurich in
Switzerland. "This is a very important study."

Different damage

The study is the result of more than a decade's work by Collinge and his
team. They tested the susceptibility of the mice by injecting vCJD
prions into the brains of mice. The prions are thought to alter the
proteins produced by MM genes, causing them to clump together and giving
the brain a 'spongy' appearance. But the brains of animals lacking the
MM genes also became spongy and showed clumps of altered protein
characteristic of prion disease, although the distribution of these
effects was different from that seen in MM mice with vCJD.

Researchers say the results suggest that humans without MM genes could
suffer the same kind of brain damage seen in vCJD, but in different
areas of the brain. But they warn that Collinge's work could also mean
that people without MM may simply carry the prions without developing
symptoms, or may develop similar symptoms after a longer incubation period.

"All these possibilities are up for grabs," says James Ironside,
director of the National Creutzfeldt-Jakob Disease Surveillance Unit at
the Western General Hospital in Edinburgh, UK.

Experts had already suspected that people without MM were vulnerable to
vCJD, Ironside adds. In May this year, a survey of around 13,000 tissue
samples from hospital patients revealed two cases of unusual patterns of
prion infection (see "Tissue survey raises spectre of 'second wave' of
vCJD "),
although the patients' genetic types were not known. Ironside adds that
he also saw evidence of vCJD-like infection in the autopsy of a non-MM
person from the Netherlands.

Ironside and Glatzel agree that it is too early to say whether
predictions about the course of Britain's vCJD epidemic, which appears
to be waning, should be changed in the light of Collinge's results. They
stress that tight surveillance of prion diseases needs to be maintained,
so that the brains of patients who die from the condition can be studied
for evidence of new strains of CJD.



1. Wadsworth J. D. F, et al. Science, doi:10.1126/science.1103932


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