Guest guest Posted November 14, 1998 Report Share Posted November 14, 1998 The scientists in the US and all over the world are working to try and find an answer. The simple/complicated problem is that they do not understand how it works...............Pat BSE, AUTOIMMUNE THEORY > > Date: Fri, 06 Nov 1998 11:18:00 -0800 (PST) > > > > Followers of the BSE story may be interested in this paper which proposes > an alternative hypothesis to the 'prion theory'. The authors suggest that > bacteria contain molecular sequences which resemble brain tissue and set up > an autoimmune reaction. An abstract of the paper has just been added to the > CAB ABSTRACTS database and will be available shortly. > > Bovine spongiform encephalopathy: comparison between the 'prion' hypothesis > and the autoimmune theory. Ebringer, A.; Pirt, J.; , C.; Thorpe, C.; > Tiwana, H.; Cunningham, P.; Ettelaie, C. (Division of Life Sciences, > Infection and Immunity Group and Department of Computing, King's College, > Campden Hill Road, London, UK.) Journal of Nutritional & Environmental > Medicine (1998) 8 (3), 265-276 > > Another paper by one of the authors proposing the same theory can also be > seen on the database (BSE is an autoimmune disease. The prion infectious > protein fallacy, by J. Pirt & M. W. Pirt). > > -- > > Animal Health > e-mail: R.TAYLOR@... > > *** > > [i asked Ralph Blanchfield for his comments. - MHJ] > > Date: Fri, 06 Nov 1998 19:59:15 GMT > > > > There is nothing new about this, and it has already been amply aired on > BSE-L. > > Following a lecture by Ebringer, reported in The Times around a year ago, > Ebringer and Pirt expounded their hypothesis in their evidence to the BSE > Inquiry on 26 March 1998. More recently, Pirt wrote a letter that was > published in the Society of Chemical Industry's journal, Chemistry and > Industry, on 19 October. It was also posted on BSE-L, by Paddy Apling, on > 19 October, and read as follows:- > > Prions or bacteria? > > The prion theory to account for the cause of BSE and related diseases is > referred to twice in a recent issue (C&I 1998, 714 & 726). This theory of > Prusiner has now been in existence for 16 years. However, it remains highly > controversial. One of its fundamental and unexplained flaws is that prion > protein in a test tube is not infectious. > > Two years ago the Ebringer autoimmune diseases group, of which I am a > member, at King's College, London, postulated that BSE could be not an > infectious disease but rather an autoimmune disease in which the body > produces antibodies which react with myelin and destroy the nerve cells. > > We started from the observation that injecting a minute amount of pure > myelin A1 protein (0.1?g) (or a synthetic small peptide containing the > epitope) into a rodent causes a spongiform encephalopathy (EAE). This is > indistinguishable clinically and histologically from BSE, The prion > adherents insist, without good reason, that EAE and so-called > 'transmissible' BSE must be different. EAE presents no difficulty for the > autoimmune theory. > > >From a theoretical study, the Ebringer group found molecular mimicry > between an antigen in bacteria (_Acinetobacter_ sp.) and the EAE epitope in > myelin. We predicted, therefore, that cattle with BSE or patients with CJD > would have elevated levels of antibodies to _Acinetobacter_. This > prediction has been fully confirmed. > > Hence we conclude that the BSE epidemic was started by exposure of cattle > to _Acinetobacter_ in meat and bonemeal (MBM) feed supplement, not to > prions. It is not to be ruled out that perhaps the presence of large > quantities of myelin in the MBM could have been indigestible (cattle are > supposed to be herbivores) and resulted in the uptake of myelin antigen > through the intestinal wall with consequent antibody formation. > > Unfortunately, the effect of feeding normal brain tissue to cattle has not > been tested. We predict that it would have the same effect as feeding BSE > brain tissue. We have discussed the evidence for the autoimmunity theory at > length in the BSE Inquiry (Internet, 26 March, day 11). Also the > prion and autoimmunity theories are compared by Ebringer et al (J. > Nutrition Environ. Med., 1998,8,267). > > The dispute can be resolved only by further research on the autoimmune > theory. However, the prion lobby is in control of all the government > sources of funds for research on BSE and related diseases, and vested > interests prevail. > > S Pirt London, UK > > ********** > > I sent a response to Chemistry and Industry, which I also posted on BSE-L, > on 22 October. The letter appeared (in slightly shortened form) in > Chemistry and Industry on 2 November. The version that appeared in Chem and > Ind. was as follows: > > Prions or Bacteria? > > As I am not in any way connected with any research group having or seeking > funding for research on BSE or other TSEs, perhaps I may be permitted to > comment on S Pirt's letter (C&E 1998, 826) without fear being labelled > as one of the " vested interests " to which he refers. > > It is true that the whole BSE/spongiform encephalopathy scenario is > extremely complicated and difficult to understand. It resembles a large > jigsaw puzzle in which many of the pieces are missing, and in which pieces > that appear to be adjacent parts of the picture sometimes do not seem to > fit exactly. There is a great deal more still to be learned. Having read > the evidence given at the BSE Enquiry, it is still not clear to me how > Ebringer and Pirt's hypothesis can account for the enormous difference in > BSE incidence between the UK and other countries that used MBM in cattle > feed. However, I would support the view that all plausible hypotheses in > this field should be the subject of funded research. > > It is also true that the prion hypothesis has not been proved. However, to > the unbiased observer familiar with the accumulated research literature, > particularly over the last few years, the volume of findings supporting or > consistent with the prion hypothesis is far too great to allow of its > dismissal as " highly controversial " . > > To say that " one of its fundamental flaws is that prion protein in a test > tube is not infectious " is untrue - no-one has demonstrated that to be the > case, and absence of evidence is not evidence of absence. It is true that, > so far, no-one has demonstrated the infection of an animal by purified > infectious prion protein " from a test-tube " ; but the ability of the > abnormal prion protein to convert normal prion protein to the abnormal form > has been demonstrated in vitro. > > and co-workers (Nature,1997, 388, 285-8) carried out in vitro > cell-free conversion reactions with purified and radio-labelled scrapie > and BSE prions and human prions, both met/met homozygous and val/val > homozygous at codon 129 (surprisingly they did not report having included > heterozygous at codon 129 in the experiments). They have shown that there > is a correlation between in vitro conversion efficiencies and known > transmissibilities of BSE, sheep scrapie and CJD. On this basis, they used > the in vitro system to gauge the potential transmissibility of scrapie and > BSE to humans. They found limited conversion of normal human protein to the > abnormal form driven by the abnormal protein associated with both scrapie > and BSE . > > The efficiencies of these heterologous conversion reactions were similar > but much lower than those of relevant homologous conversions. Thus the > inherent ability of these infectious agents of BSE and scrapie to affect > humans following equivalent exposure may be finite but similarly low. > Incidentally they reported that the conversion of val/val-129 was threefold > less efficient than of met/met-129, interesting when remembering that, so > far, all nvCJD victims have been met/met-129. > > Pirt also stated > > " Unfortunately, the effect of feeding normal brain tissue to cattle has not > been tested. We predict that it would have the same effect as feeding BSE > brain tissue. " > > That is incorrect. idis and idis have carried out control > experiments with uninfected brain tissue, and they did not result in TSEs > (Proc. Nat. Acad.Sci. USA, 1993, 90(16), 7724-8 > > J Ralph Blanchfield Chingford, UK Quote Link to comment Share on other sites More sharing options...
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