By RANDOLPH
E. SCHMID
Associated Press Writer
WASHINGTON
(AP)--Researchers were able to delay the onset of a form of mad cow disease by
blocking a protein that usually assists the immune system.
In the end,
scrapie, the form of the disease that affects sheep and is not transmittable to
humans, did develop in the test mice, but the work may point the way for further
research into battling the illness. The findings are reported in the April issue
of the journal Nature Medicine.
The course of mad cow diseases is not
fully understood, but victims appear to become infected by eating food contaminated
with a rogue protein called a prion, which then reproduces in the lymph system
before moving into the brain.
A team of researchers in the United Kingdom,
led by Neil A. Mabbott of the Institute for Animal Health in Edinburgh, Scotland,
was seeking to learn if complement factors--proteins in the immune system--had
a role in the disease development.
They knew that cobra venom factor depletes
some of these complement proteins, so they treated mice with it and then infected
them with scrapie.
``In our study, treatment with cobra venom factor lead
to a highly significant delay in the onset of scrapie in mice by delaying the
spread of disease to the brain,'' Mabbott said.
The disease eventually
did develop and the mice died, but the onset of symptoms was delayed by 24 days,
he said.
``While we are not advocating that people or animals should be
treated with cobra venom factor, our findings suggest that complement inhibitors
may present an opportunity for early therapeutic intervention in these diseases,
in the interval between exposure to infection'' and invasion of the brain, Mabbott
said.
Mad cow disease and scrapie are part of a family of diseases called
transmittable spongiform encephalopathy. Variant Creutzfeldt-Jakob disease in
humans has been linked directly to eating meat from cattle infected with mad cow
disease. Scrapie is not transmittable to humans.
In a separate paper in
the same issue of Nature Medicine a team led by Michael A. Klein of the University
of Zurich, Switzerland, also reported that mice who were missing some complement
factors in their immune systems were temporarily protected from scrapie, with
development of the disease delayed.
But there are problems to be resolved.
The delayed but eventual development of the disease may indicate that
there are multiple ways for the disease to move into the brain, noted Franco Cardone
and Maurizio Pocchiari of the Virology Laboratory of the Instituto Superiore di
Sanita in Rome, Italy.
In addition, to delay the disease the complement
inhibitor needs to be used before symptoms develop. That could be done in the
lab because Mabbott's team knew when the mice would be injected with scrapie.
But pursuing such treatment in other animals or people would depend on finding
ways to diagnose the infection before symptoms develop, Pocchiari and Cardone
wrote. |
