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##################### Bovine Spongiform Encephalopathy ##################### UNITED STATES DISTRICT COURT FOR THE DISTRICT OF MONTANA BILLINGS DIVISION ) RANCHERS CATTLEMEN ACTION LEGAL FUND ) UNITED STOCKGROWERS OF AMERICA, ) ) Plaintiff, ) ) v. ) ) UNITED STATES DEPARTMENT OF AGRICULTURE, ) Cause No.CV-05-06-BLG-RFC ANIMAL AND PLANT HEALTH INSPECTION ) SERVICE, et al., ) ) Defendants ) ) DECLARATION OF STANLEY B. PRUSINER, M.D. Stanley B. Prusiner, M.D. certifies and states as follows: 1. I submit this declaration in connection with R-CALF USA’s motion for summary judgment in the above-captioned action. It is based on my own personal research and on my familiarity with research performed by others, including the scientists working in the laboratory that I oversee. 2. I am the Director of the Institute for Neurodegenerative Diseases and a Professor of Neurology and Biochemistry at the University of California, San Francisco (UCSF). I am also the founder of InPro Biotechnology, Inc. 3. In 1997, I was awarded the Nobel Prize in Physiology or Medicine for my discovery of the novel protein agent, which I named "prions," that are the cause of transmissible spongiform encephalopathies (TSEs), or prion diseases, such as bovine spongiform encephalopathy (BSE). 4. I am a member of a number of learned societies including the National Academy of Sciences, the Institute of Medicine, the American Academy of Arts and Sciences, and the American Philosophical Society. I am also a foreign member of the Royal Society, London. 5. I am the editor and a contributing author of Prion Biology and Diseases, which was published in 1999 to encourage young scientists to enter the field of prion biology, as well as to serve as a reference source for senior investigators. The second edition of Prion Biology and Diseases was published in 2004 to document the substantial advances that have been made in prion research since 1999. In addition to Prion Biology and Diseases, I am the editor of ten books and an author of hundreds of scientific articles in peer- reviewed journals and book chapters. A complete list of my publications is contained in my curriculum vitae which is attached to this declaration as Appendix A. 6. In 1964, I graduated with an A.B. (cum laude) from the University of Pennsylvania in Philadelphia, Pennsylvania. In 1968, I earned my M.D. from the University of Pennsylvania School of Medicine. From 1969 until 1972, I served as Research Associate with the rank of Lt. Commander in the U.S. Public Health Service at the National Institutes of Health, National Heart and Lung Institute, Laboratory of Biochemistry, Section on Enzymes, Bethesda, Maryland. From 1972 until 1974, I completed my residency in Neurology at UCSF. 7. From 1974 until 1980, I served as Assistant Professor of Neurology at UCSF. Between 1976 and 1988 I was a lecturer in the Department of Biochemistry and - 2 - Biophysics at UCSF. From 1979 until 1983, I was Assistant Professor of Virology in Residence at the University of California, Berkeley (UC Berkeley). In 1980 and 1981, I was Associate Professor of Neurology in Residence at UCSF. From 1981 until 1984, I was Associate Professor of Neurology at UCSF and from 1983 until 1984, Associate Professor of Virology in Residence at UC Berkeley. In 1984, I was appointed Professor of Neurology at UCSF and Professor of Virology in Residence at UC Berkeley. In 1988, I was appointed Professor of Biochemistry at UCSF. 8. In September 1972, two months after I began my residency at UCSF in the Department of Neurology, I admitted a female patient who was exhibiting progressive loss of memory and difficulty performing some routine tasks. I was surprised to learn that she was dying of a "slow virus" infection called Creutzfeldt-Jakob disease (CJD), which evoked no response from her body’s defenses. Next, I learned that scientists were unsure if a virus was really the cause of CJD since the causative infectious agent had some unusual properties. The amazing properties of the presumed causative "slow virus" captivated my imagination and I began to think that defining the molecular structure of this elusive agent might be an intriguing research project. The more that I read about CJD and the seemingly related diseases, such as kuru in the Fore people of New Guinea and scrapie in sheep, the more captivated I became. 9. My research is focused on infectious proteins called prions that cause fatal neurodegenerative diseases including BSE in cattle, scrapie in sheep, chronic wasting disease in deer and elk, and CJD in humans. Nascent prions are created by (1) spontaneous (or sporadic) refolding of a host protein, (2) genetic mutation or (3) exposure to exogenous prion. In mammals, prions are composed of a modified form of the prion - 3 - protein (PrP) designated PrPSc (the superscript "Sc" is for scrapie which is the most wellstudied prion disease). Like other infectious pathogens, prions multiply but they do not have a nucleic acid genome to direct the synthesis of their progeny. Rather, PrPSc (or prions), can induce the normal, cellular prion protein, designated PrPC, to refold. In doing so, it becomes infectious. The mis-folded prion proteins (PrPSc) can build up, creating masses of protein that rupture cells and cause microscopic holes in the brain. The destruction is so severe that the brain begins to resemble a sponge and death is certain. Prion diseases of humans and animals are 100% fatal. No vaccines, antidotes or cures exist to treat these disorders. 10. Since this structural transition in the prion protein underlies both the replication of prions and the pathogenesis of Central Nervous System (CNS) degeneration, much of the effort in my laboratory is devoted to elucidating the molecular events responsible for this process. Indeed, prion diseases seem to be disorders of protein conformation. 11. As a result of the unusual nature of prion diseases (e.g., the very small exposure to prions that can cause disease; resistance to heat, irradiation, and chemicals that might destroy or modify nucleic acids; incubation in animals and humans for years without any symptoms), controlling prion diseases is very difficult. Policy makers need to take immediate and aggressive measures to minimize and mitigate the risk of prion transmission between animals and humans. In doing so, this will ensure the safety of our food supply. 12. Evidence from numerous scientific studies supports the conclusion that a variant of Creutzfeldt-Jakob disease (vCJD), can be caused by ingestion of BSE-infected beef and beef products. Approximately 170 cases of vCJD have been attributed to - 4 - consumption of BSE-tainted beef and beef products (occurring primarily in the United Kingdom (UK)). It is unknown how many other people worldwide are harboring prions that cause vCJD. Some scientists have projected the possibility that thousands of people may be infected with vCJD prions. Recent testing of tonsils and appendices removed from otherwise-healthy individuals in the UK argues that thousands of people may be harboring vCJD prions from the consumption of BSE-infected beef. It is important to note that there is evidence of two iatrogenic transmissions of vCJD prions from human to human, to date. 13. Many researchers believe that there is a "species barrier," meaning that humans are less susceptible than cattle to the prions causing BSE and vCJD. Comparing known cases of vCJD to estimated exposures to BSE-contaminated meat is not sufficient to establish that there is a species barrier for several reasons: First, the incubation period for prion diseases in humans typically is long (anywhere from two and up to as many as 40 years), thus there may be many individuals with vCJD prions who are currently asymptomatic. Second, many scientists are concerned that vCJD is under-diagnosed, given the unusual nature of the pathogen, the difficulty of an accurate diagnosis short of an autopsy, and that prion science is a relatively new field of study. Finally, the denominator in any estimate of a species barrier – the amount of infected tissue to which humans were exposed – can only be an approximation, based on limited test data and many assumptions. Risk assessment and risk management decisions about the safety of our food supply should be based on the concept that one infectious unit (or dose) of prions is sufficient to cause vCJD in humans. - 5 - 14. In vCJD, prions accumulate not just in the brain and spinal cord but also in the lymphoid tissues, such as the tonsils and appendix, suggesting that prions enter the bloodstream. Sheep and rodent studies have shown that prions can be transmitted to healthy animals through blood transfusions from infected animals. Two recent cases in the UK argue that vCJD prions were transmitted between humans through blood transfusions. Because there is no reason to believe that BSE prions in cattle behave differently from those in other mammals, feeding bovine blood to cattle presents a risk of transmission of BSE prions. Therefore, a program to minimize the propagation of BSE prions should include, but not be limited to, a ban on feeding ruminant blood to other ruminants and to animals, a practice which I understand has been advocated by the U.S. Food and Drug Administration. 15. Given the evidence that prions are found in blood, prions may be present in any organ including muscle, since all tissues are perfuse with blood. Patrick Bosque (now at the University of Colorado’s Health Sciences Center) and I found prions in the hind limb muscles of mice at a level approximately 100,000-fold higher than that found in blood. Michael Beekes and his colleagues at the Robert Koch Institute in Berlin discovered high-levels of prions in virtually all skeletal muscles, not just in the hind limbs, after prions were fed to hamsters; and other scientists have found prions in the tongues of infected hamsters. Sheep infected with scrapie prions were found to have prions in both the hind and fore limb muscles. Similar findings have been observed in humans with CJD. My UCSF colleagues Jiri Safar and Stephen DeArmond found prions in the muscles of CJD patients, and Adriano Aguzzi and his colleagues at the University of Zürich identified prions in the muscles of 25% of the CJD patients they examined. - 6 - 16. Based on these and other scientific studies, it is reasonable to contend that the consumption of beef and beef products from cattle harboring BSE prions presents a risk for humans. Regardless of whether the tonsils and distal ileum have been removed from cattle – and in the case of cattle 30 months of age and older, the brain, eyes, spinal cord, and trigeminal ganglia as well – these measures are unlikely to be sufficient to ensure the safety of the meat we consume. The only reliable way to minimize the risk of humans developing vCJD from BSE-infected cattle is to eliminate BSE-infected cattle from the food chain. And the only way to reduce the number of BSE-infected cattle entering the food chain is to require blanket testing of all slaughtered cattle so that animals testing positive for prions will be removed from the food supply. 17. Since the mid-1980s, scientists at my laboratory and around the world have attempted to develop methods for identifying prions that can serve as an alternative to the immunohistochemistry test (IHC). The IHC test can be unreliable, cumbersome and extremely time-consuming. For example in a recent publication by my colleagues Safar and DeArmond, IHC consistently detected prions in only 4 out of 18 regions (22%) in human CJD brains whereas the CDI (Conformation-Dependent Immunoassay) test developed at UCSF detected prions in all 18 regions (100%). IHC is routinely used by the USDA as their confirmatory test and is considered their "gold standard." More streamlined and sensitive methods have been developed to conduct broader and more accurate testing for prions including the CDI. A significant portion of my career has been dedicated to the development and evaluation of sophisticated techniques for the detection of prions and subsequent diagnosis of BSE, scrapie, sporadic CJD and vCJD. A company - 7 - I founded, InPro Biotechnology, offers several sensitive and reliable prion tests which are being made available commercially. 18. It has been confirmed that two Japanese cows were diagnosed with BSE at 21 and 23 months of age in the fall of 2003. These cases help to demonstrate the necessity of blanket testing of all cattle at slaughter, including the testing of cattle less than 30 months of age. Neither of these two Japanese cows showed clinical signs of neurological dysfunction, thus neither would have been selected as a "high-risk" animal and designated for testing under current USDA protocols. These cows were only identified as positive for BSE prions because of the Japanese government's decision to adopt a policy of blanket testing for BSE at slaughter. 19. Experience in Europe has shown that, when countries have switched from only testing cattle showing clinical signs of neurological disorders to testing all animals above a certain age, the number of reported BSE cases increases. The European Union (EU) adopted regulations in 2001 requiring BSE screening of all animals over 30 months of age intended for the human food supply. (France, Germany, Italy and Slovenia choose to test all cattle that are over 24 months of age.) A May 2004 report from the EU Health and Consumer Protection Directorate-General shows that, as a result of testing all cattle slaughtered for human consumption above a specific age, more cases of BSE have been identified through this "active" testing than were identified through the testing of cattle that were determined by farmers or veterinary practitioners to exhibit clinical signs for BSE (referred to as "passive" testing). This active testing in the EU has shown that BSEinfected cattle may display no signs even though they harbor substantial numbers of prions that can be identified using a rapid test for BSE. Thus, active testing of cattle - 8 - slaughtered for human consumption has prevented BSE-infected cattle from entering the food chain. The rapid BSE tests that are currently available, as well as those that are becoming available, are sensitive enough to make universal screening for BSE practical, without imposing excessive costs. 20. Current scientific knowledge demonstrates the ability to detect prions in cattle less than 30 months of age: BSE prions were detected in two cows 21 and 23 months of age in Japan. In the UK, 84 cases of BSE have been found in cattle 30 months of age and younger. Two positive animals under 30 months of age have also been detected in Germany. Recent advances in BSE diagnostics including tests developed in my laboratory at UCSF are the most likely to detect low-levels of prion infectivity. In order to realize the human-health benefit of testing it will be important to utilize the most sensitive and specific detection methods available. We should not underestimate the value of removing all apparently healthy cattle with detectable levels of BSE prions from the food chain. Such animals do not exhibit clinical signs and thus, would not otherwise be excluded from the food supply. I believe that testing all slaughtered animals is the only rational policy for adequately protecting the human food supply. 21. Given that no country other than Japan routinely screens cattle of all ages entering the food supply, and that only France, Germany, Italy, and Slovenia require routine BSE testing of cattle beginning at 24 months of age, there is little empirical data on BSE in younger cattle. Because the amount of infected tissue necessary to cause vCJD in humans is not known, and because the distribution of prions in infected cattle over time is not completely understood, it is neither safe nor scientifically justified to assume that all - 9 - - 10 - http://www.r-calfusa.com/BSE/06-28-05%20--%20Prusiner%20Declaration%20(10%20pgs).pdf Testimony, Legal Filings, and Studies Prusiner Declaration (Adobe Acrobat PDF File 238K) http://www.r-calfusa.com/BSE/06-28-05%20--%20Prusiner%20Declaration%20(10%20pgs).pdf Cox Declaration (Adobe Acrobat PDF File 90K) http://www.r-calfusa.com/BSE/06-28-05%20--%20Tony%20Cox%20Declaration%20(47%20pgs).pdf Charnley Declaration (Adobe Acrobat PDF File 17K) http://www.r-calfusa.com/BSE/06-28-05%20--%20Charnley%20Declaration%20(6%20pgs).pdf Weaver Declaration (Adobe Acrobat PDF File 33K) http://www.r-calfusa.com/BSE/06-28-05%20--%20Weaver%20Declaration%20(12%20pgs).pdf R-CALF USA's reply to USDA's cross motion for summary judgment (Adobe Acrobat PDF File 51K) http://www.r-calfusa.com/BSE/062805%20RC%20Reply%202%20USDAs%20Cross%20Motion%204%20Summary%20Judgment.pdf #################### https://lists.aegee.org/bse-l.html #################### WELL, i am nobody, i have no PhDs, and i am president and ceo of nothing, but i can tell you this much ; https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 PART 2 PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ... http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt # Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. 03N-0009 Federal Preemption of State & Local Medical Device Requireme. ... Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater Comment Number: EC -1 Accepted - Volume 1 ... 00D-1662 Use of Xenotransplantation Products in Humans. http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm 2003D-0186 01N-0423 Substances Prohibited from use in animal food/Feed Ruminant APE 5 National Renderers Association, Inc. Vol#: 2 APE 6 Animal Protein Producers Industry Vol#: 2 APE 7 Darling International Inc. Vol#: 2 EMC 1 Terry S. Singeltary Sr. Vol#: 3 http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm Send Post-Publication Peer Review to journal: disease in the United States I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? LANCET INFECTIOUS DISEASE JOURNAL My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem. largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation. occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally , he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle. transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive. is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk. issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE. teeth , Singeltary argues. You get it when they want you to have it, and only what they want you to have. University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings ; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure . The USA should develop a system modelled on that established in the UK, he points out. Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans ; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further . Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison. the [Samii] cases because there is no evidence that the men ate CWD-infected meat . He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited . Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. <<< actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article... Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama BRITISH MEDICAL JOURNAL SOMETHING TO CHEW ON BMJ http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2 BMJ http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 THE PATHOLOGICAL PROTEIN BY Philip Yam Yam Philip Yam News Editor Scientific American www.sciam.com IN light of Asante/Collinge et al findings that BSE transmission to the -------- Original Message -------- Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43 -0000 From: "Asante, Emmanuel A" To: Dear Terry, I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention. Thank you for your interest in the paper. In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc. I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes. Emmanuel Asante <> ____________________________________ Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now) ____________________________________ snip... full text ; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Creutzfeldt-Jakob disease THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible http://www.pnas.org/cgi/content/full/041490898v1 Characterization of two distinct prion strains http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471 ALL human TSEs must be made reportable Nationally and Internationally, of all ages...TSS
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