Elliot Morley and TSE
Originally from: Joyce
Mona, did you post something this week ....a comment from Elliot Morley about TSE's and environmental causes? I have seen it somewhere and can't find it on the message board or on warmwell.
Anyone else know?
Joyce
Originally from: Joyce
Thanks Bill, how could I mix you up with Mona lol!
Please could you send it to Mark Purdey also?
Joyce
Originally from: Bill
It was from me Joyce. I will transcribe the letter and post it on here. Bill.
Originally from: Bill
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.








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