This is a transcript of the letter from Elliot Morley in response to my
concerns about TSE research. The letter is addressed to my M.P., Nigel Evans.

Thank you for your letter of 4 December to Margaret Becket, enclosing one from W M Snape. I am sorry for the delay in replying.

The Department maintains an awareness of the latest research on TSEs and the
prion protein. We commission research to investigate the nature of the
infective agent and are informed by research conducted around the world. In
addition, the Spongiform Advisory Committee (SEAC), which advises the
Government on these matters, is comprised of scientists who are active in
research on various aspects of these diseases. It is true to say, therefore,
that the Department is fully informed on the science of TSEs and the prion
protein.

The mechanisms by which the prion protein is converted from a normal to an
abnormal form are still poorly understood. Even less clear is how abnormal
prion protein 'replicates'. As no TSE-specific nucleic acid associated with
infection has been identified, hypotheses for prion 'replication' involve
protein only models. Such hypotheses are being investigated by many groups
world-wide. However, it is true to say that much remains to be learnt about
this feature of the disease.

The abnormal prion protein is indeed resistant to normal biochemical
breakdown and thus forms aggregates in the brain. However it is not known
whether death is caused by the aggregation of prions or some other feature of
the infection.

The concept of genetic susceptibility/resistance is becoming increasingly
better understood, especially in sheep, where certain genotypes have been
shown to be more resistant to scrapie infection than other genotypes. Sheep
with resistant genotypes are found all over the country and have been present
in the national flock for a great many years. It is therefore unlikely that
there is a significant effect of nutrition on susceptibility. New Zealand
sheep have been used in experiments to investigate the effects of genotype on
disease susceptibility, because the New Zealand flock is scrapie free.

Valid theories for the cause of TSEs must take into account the existence of
a replicating, transmissible agent. Whilst there is no experimental support
for the possibility that an environmental factor triggers the formation of a
novel transmissible agent, there is limited experimental evidence to suggest
that environmental factors could affect susceptibility to TSEs. However, no
environmental factors have so far been found to affect the susceptibility of
cattle to BSE. Indeed, the evidence that BSE in cattle was caused and spread
through the feeding of infected meat and bone meal is overwhelming.

I am aware that Lord Whitty has responded to Mr. Snape's comments on Foot and
Mouth Disease testing in several previous letters, most recently in November
of this year. I do not think there is anything further I can add on this
subject.

ELLIOT MORLEY.