Recommendation of the Swiss Expert Committee for Biosafety on the 
classification of activities using prion genes and prion protein 
January 2013 
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Content 
Introduction 
................................................................................................................................ 
3 
Legal 
bases................................................................................................................................ 
3 
Safety measures for work using TSE 
agents.............................................................................. 
3 
Risk assessment for work with prion proteins and prion 
genes................................................... 4 
Classification of work with TSE 
agents....................................................................................... 
4 
References................................................................................................................................. 
7 
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Introduction 
Prions (proteinaceous infectious particles) cause neurodegenerative 
diseases such as Creutzfeldt-Jakob Disease (CJD) and Kuru in humans, and Bovine 
spongiform encephalopathy(BSE) and scrapie in animals. The umbrella term for 
these diseases is transmissible spongiform encephalopathy (TSE), which is used 
in this Recommendation. A prion originates in a PrP gene.The transcription and 
translation of this gene generates the physiologically apathogenic PrPprotein 
(PrPc; c = cellular). The essential, or possibly the only, component of a prion 
is apathologically misfolded form of the PrP protein, PrPsc (sc = 
scrapie-associated). PrPsc in turn leads to a further refolding of PrPc to 
PrPsc, producing an autocatalytic chain reaction. Thus PrPsc collects in the 
affected tissues, primarily in the brain, sometimes leading to irreversible 
lethal pathological changes. Prions can be transmitted orally, iatrogenically or 
via wounds. Thus persons who handle prions are at risk of becoming infected, 
with a TSE as a consequence. 
Legal bases 
• Agents causing TSE are classified under group 3** (FOEN Classification of 
Organisms. Module 2: Viruses; December 2011). 
• The term group 3** is used for organisms that possess a limited risk of 
infection to workers because air-borne transmission, according to current 
scientific knowledge, cannot normally occur. Transmission can only take place 
through contact with infected tissue, body fluids or contaminated medical 
instruments. 
• It is now certain that humans can become infected through the oral uptake 
of a BSE pathogen. Thus, work must be carried out in laboratories of level 3**, 
although the omission of particular safety measures may be requested (see below) 
• No link to human TSEs has yet been shown for other animal TSEs (scrapie, 
chronic wasting disease (CWD)). The safety measures of a level 2 laboratory are 
therefore sufficient. 
Safety measures for work using TSE agents 
• The laboratory must satisfy the safety measurements of level 3; the 
omission of particular safety measures may however be requested (see below). 
• An airlock with washing and disinfection facilities must be available, 
but a shower is not necessary. 
• All studies in which aerosols may be produced must be performed in a 
class II microbiological safety cabinet. 
• An autoclave must be able to reach temperatures of 134°C (validated). It 
must also be available in the same laboratory if possible, or at least in the 
same building. 
• Wastes and waste water must be decontaminated. 
• A list of the laboratory personnel who have been in contact with prions 
must be kept for at least the period prescribed in the Contain O and the PEMO. 
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Measures that could be omitted when working with prions, since the danger 
to the environment is relatively small: 
• Filtration of air exiting the laboratory with a HEPA filter 
• Negative air pressure in the laboratory 
• Ability to seal the area for gassing, since prions cannot be destroyed by 
gas (e.g.formaldehyde). Risk assessment for work with prion proteins and prion 
genes The following findings from scientific research must be borne in mind when 
the risks associated with handling prions are being assessed. Studies with 
native and with mutant recombinant prion proteins are also included in the 
considerations. 
• Experimental studies on scrapie in mouse and in hamster have been carried 
out for several decades. There are no indications that the scrapie agent 
represents an increased risk either for occupationally exposed persons or for 
the public and the environment. To date, it has not been demonstrated that 
scrapie can be transmitted to humans. However, rodents infected with scrapie 
agents should be handled using the same safety precautions as rodents infected 
with natural, mouse-specific pathogens (classified into group 2). 
• It has been shown that the primary structure of the prion protein plays 
an important role in transmission of prions from one species to another 
(Prusiner et al., 1990; Colby et al.,2011). The sequence of the bovine PrP gene 
shows greater homology to the sequence of the human gene than the sequence of 
the mouse or hamster gene (Gabriel et al., 1992).Although it is possible to 
transmit bovine TSE agents to humans, it appears unlikely that mouse- or 
hamster-specific TSE agents can be transmitted to humans. 
• It is now possible to transform native recombinant PrPc or PrPc from 
tissue extracts into infectious prions (PrPsc). Particularly when using PMCA 
technology (Protein Misfolding Cyclic Amplification), infectious prions 
reproduce efficiently in the laboratory (Castilla et al.,2005; Wang et al., 
2010). It is vital that this be taken into account in the risk assessment. 
• Certain activities using PrP genes should be treated with caution. 
Bearing in mind the current gaps in knowledge, the following activities present 
an increased risk to humans and the environment: (1) cloning of PrP genes in 
host organisms that could replicate in/on humans, and (2) the cloning and 
expression of modified PrP genes in prokaryotic and eukaryotic expression 
systems where there is a possibility of producing infectious PrPSc. 
• Mutations in the DNA sequence of the PrP gene, without a host organism, 
poses a negligible risk according to the current state of science. This activity 
may thus be classified under Class 1. Classification of work with TSE agents 
Based on the risk assessment above, the following recommendations can be made 
for work with prions and prion proteins (see also Table on p. 5): 
Animals 
• Autopsy of sick cattle should be done in accordance with the Epizootic 
Diseases Ordinance and according to special clinical regulations, in principle 
using the safety measures of level 2(see Diagram on p. 6). Infected cattle used 
for research purposes can be kept in safety level 1, since transmission via 
aerosol can be virtually ruled out. 
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• Activities with animals infected with rodent-adapted scrapie prions, i.e. 
animal husbandry and care, invasive procedures (e.g. inoculation with prions), 
and post-mortem examinations and tissue sampling from animals, are classified as 
class 2. 
• Activities with live mice and hamsters infected with BSE prions, 
BSE-related prions or human TSE agents (e.g. animal husbandry and care), are 
classified as class 2. The risk of bite and scratch wounds is reduced by 
handling the animals with long, blunt forceps.Invasive procedures (e.g. 
inoculation with TSE agents) as well as post-mortem examinations of infected 
animals and tissue sampling are classified under class 3. 
Tissue 
All experimental studies involving lymphoid and neural animal tissue that 
contains rodent-adapted scrapie prions are classified as class 2. Activities 
using tissue from humans and animals that contains human or bovine TSE agents 
are classified as class 3. 
Classification of work using genetically modified PrP genes and proteins 
Origin of the PrP genes 
sheep, rodent cattle, human 
Cloning of DNA in plasmid with inactive promoter 1 1 
State of the protein 
PrPc PrPSc PrPc PrPSc 
Expression in prokaryotic and eukaryotic expression systems that replicate 
in/on humans 1 2 1 2 
Expression in hosts that replicate in/on humans 1 2 2 3 
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Overview of the classification of pathological work using prions 
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References
• Advisory Committee on Dangerous Pathogens, Spongiform Encephalopathy 
Advisory Committee. Transmissible spongiform encephalopathy agents: safe working 
and the prevention of infection. London (1990). HSE Books, PO Box 1999, Sudbury, 
Suffolk CO106FS.
• Prusiner SB, Scott M, Foster D, Pan KM, Groth D, Mirenda C, Torchia M, 
Yang SL, SerbanD, Carlson GA, et al. Transgenetic studies implicate interactions 
between homologous PrP isoforms in scrapie prion replication. Cell 63, 673-86 
(1990). 
• Colby DW and Prusiner B. De novo generation of prions. Nature 9, 771-777 
(2011).
• Gabriel JM, Oesch B, Kretzschmar H, Scott M, Prusiner SB. Molecular 
cloning of a candidate chicken prion protein. Proc Natl Acad Sci U S A 89, 
9097-101 (1992).
• Council Directive of 26 November 1990 on the protection of workers from 
risks related to exposure to biological agents at work of 26 November 1990 
(90/679/EEC). Official Journal of the European Communities No. L 374/1 of 
31.12.1990, and modifications up to and including 6.12.1997 (97/65/EC). 
• Risk assessment of laboratories involving the manipulation of 
unconventional agents causing TSE. (2009) isp/wiv.
• Guidance from the ACDP TSE Risk Management Subgroup http://www.dh.gov.uk/ab/ACDP/TSEguidance/index.htm 
• Castilla et al. In vitro generation of infectious scrapie prions (2005) 
Cell 121, 195-206
• Deleault et al. Formation of native prions from minimal components in 
vitro (2007) PNAS104, 9741-9746
• Wang et al. Generating a prion with bacterially expressed recombinant 
prion protein (2010)Science, 327, 1132-1135 
Classification of activities using prion genes and ... - EFBS - admin.ch 
TSE Transmissible spongiforme encephalopathic agents
Biological agents associated with transferable spongiform encephalopathies 
are classified as 3**. 
Work with these agents must be done according to safety level 3, though 
certain level 3 measures can be omitted (see Classification of work using prion 
genes and prion proteins, www.efbs.ch ). 
Classification of Organisms. Part 2- Viruses. Status January 2013 
Sunday, October 27, 2013 
A Kiss of a Prion: New Implications for Oral Transmissibility 
From: Terry S. Singeltary Sr. 
Sent: Monday, October 28, 2013 11:48 AM 
Subject: 
Re: [CJDVoice] A Kiss of a Prion: New Implications for Oral 
Transmissibility 
hi xxxxx,
no, I can’t really put your mind to rest xxxxx. wish I could. I believe the 
kiss of the prion was done several years ago. the deaths of cjd to man and wife, 
man and cat, friend friend and friend, ....as with what Brown et al stated with 
the man and his wife i.e. ‘ therefore, we are left with the unanswerable 
alternatives of human-to-human transmission or the chance occurrence of sporadic 
CJD in a husband and wife.’ it is what it is, however, I would not loose any 
sleep over it. we are (in my opinion), exposed to the TSE prion in so many 
different ways in every day life. the potential for exposure and then becoming 
infected via taking care of a loved one with TSE prion disease, in my opinion 
risk factor there from is minimal, if proper precautions are taken, and even if 
they were not, the chance of becoming infected from a kiss, or casual contact is 
low, but I do not think it is zero, actually, far from it. I put this all 
together for a documentation of the known facts to date, of the potential casual 
human to human transmission. I did not put it together to scare anyone. with 
aerosol transmission of the TSE prion a reality now, infectivity in urine and 
feces and transmission there from being reality now with the TSE prion disease, 
I don’t see how anyone can rule _out_ the potential for transmission of the TSE 
prion via a kiss (a vehicle for transmission of the TSE prion via saliva), or 
even for a cut or open wound (all a cut is and transmission there from, is an 
crude inoculation of sorts, and inoculation has been proven to be an efficient 
mode of transmission for the TSE prion disease), even the eye, from either one 
of the body fluids now that how proven to be infections. I can’t see why we have 
such safety protocols for laboratory workers working with the TSE prion disease, 
but yet the same officials will say it’s o.k. for the public, friends, and or 
family members to do just the opposite with their loved ones when succumbing to 
the CJD TSE prion disease. don’t get me wrong, I did it too, and would probably 
do it again as far as kissing my mom. but science is science, and the 
transmission studies speak for themselves with the bodily fluids. simply put, 
which is all I was saying, we can’t say never, and or that none of these cases 
to date, have not been, and or will not be, a potential vehicle for 
transmission. I believe, and this is my opinion, that more concern for casual 
transmission with body fluids and materials there from, should be put forth to 
families with their loved ones, and I think that the safety protocols there from 
should be revised, to match that of the laboratory settings. again, this is my 
opinion. your opinion, and or others here, may read the same science and feel 
different out the findings. ...take care, kind regards, terry 
 SUBSTANCE DATA SHEET
HUMAN PRION AGENTS
FOR USE IN RESEARCH LABORATORIES
SECTION I - INFECTIOUS AGENT
Name: Creutzfeldt-Jakob agent, Kuru agent
Synonym or Cross Reference:: Subacute spongiform encephalopathy, 
Creutzfeldt-Jakob disease (CJD), Kuru, Transmissible Spongiform Encephalopathy 
(TSE).
Characteristics: Filterable, self-replicating agent, slow infectious 
pathogen, prion protein (PrP)
SECTION II - RECOMMENDED PRECAUTIONS
Containment Requirements: Biosafety level 3 facilities, practices and 
containment equipment for activities involving these agents; also listed under 
biosafety level 2 with special precautions; level of containment will depend on 
the nature of the manipulations and the amount of sera, bio/necropsy materials 
handled
Protective Clothing: Gown and gloves when handling potentially infectious 
materials; eye protection may also be indicated
Other Precautions: Extreme care must be taken to avoid accidental 
autoinoculation or other parenteral inoculations of infectious tissues and 
fluids
SECTION III - HANDLING INFORMATION
Spills: Allow any potential aerosols to settle; wearing protective 
clothing, gently cover spill with paper towel and apply 1N sodium hydroxide, 
starting at perimeter and working towards the center; allow sufficient contact 
time (1 hour) before clean up
Disposal: Decontaminate before disposal; steam sterilization (132·C for 1 
hour), disinfection with 1N sodium hydroxide for 1 hour, incineration
Storage: In sealed containers that are appropriately labeled 
The main precaution to be taken by laboratorians working with 
prion-infected or contaminated material is to avoid accidental puncture of the 
skin.3 Persons handling contaminated specimens should wear cut-resistant gloves 
if possible. If accidental contamination of unbroken skin occurs, the area 
should be washed with detergent and abundant quantities of warm water (avoid 
scrubbing); brief exposure (1 minute to 1N NaOH or a 1:10 dilution of bleach) 
can be considered for maximum safety.6 Additional guidance related to 
occupational injury are provided in the WHO infection control guidelines.6 
Unfixed samples of brain, spinal cord, and other tissues containing human prions 
should be processed with extreme care in a BSL-2 facility utilizing BSL-3 
practices. 
Bovine Spongiform Encephalopathy Although the eventual total number of 
variant CJD cases resulting from BSE transmission to humans is unknown, a review 
of the epidemiological data from the United Kingdom indicates that BSE 
transmission to humans is not efficient.9 The most prudent approach is to study 
BSE prions at a minimum in a BSL-2 facility utilizing BSL-3 practices. When 
performing necropsies on large animals where there is an opportunity that the 
worker may be accidentally splashed or have contact with high-risk materials 
(e.g., spinal column, brain) personnel should wear full body coverage personal 
protective equipment (e.g., gloves, rear closing gown and face shield). 
Disposable plasticware, which can be discarded as a dry regulated medical waste, 
is highly recommended. Because the paraformaldehyde vaporization procedure does 
not diminish prion titers, BSCs must be decontaminated with 1N NaOH and rinsed 
with water. HEPA filters should be bagged out and incinerated. Although there is 
no evidence to suggest that aerosol transmission occurs in the natural disease, 
it is prudent to avoid the generation of aerosols or droplets during the 
manipulation of tissues or fluids and during the necropsy of experimental 
animals. It is further strongly recommended that impervious gloves be worn for 
activities that provide the opportunity for skin contact with infectious tissues 
and fluids. 
The main precaution to be taken when working with prion-infected or 
contaminated material is to avoid puncture of the skin. If accidental 
contamination of skin occurs, the area is swabbed with In sodium hydroxide 
(NaOH) for 5 minutes and then washed with copious amounts of water. Unfixed 
samples of brain, spinal cord, and other tissues containing human prions should 
be processed with extreme care at BSL 3.
Prions are characterized by extreme resistance to conventional inactivation 
procedures including irradiation, boiling, dry heat, and chemicals (formalin, 
betapropiolactone, alcohols). Sterilization of rodent brain extracts with high 
titers of prions requires autoclaving at 132C for 4.5 hours. Denaturing organic 
solvents such as phenol or chaotropic reagents such as guanidine isothiocyanate 
or alkali such as NaOH can also be used for sterilization. Disposable 
plasticware, which can be discarded as a dry waste, is highly recommended.
Although there is no evidence to suggest that aerosol transmission occurs 
in the natural disease, it is prudent to avoid the generation of aerosols or 
droplets during the manipulation of tissues or fluids and during the necropsy of 
experimental animals. Formaldehyde-fixed and paraffin-embedded tissues, 
especially of the brain, remain infectious. Some investigators recommend that 
formalin-fixed tissues from suspected cases of prion disease be immersed for 30 
min in 96% formic acid or phenol before histopathologic processing, but such 
treatment may severely distort the microscopic neuropathology. 
another interesting aspect of the TSE prion disease is KURU ; 
Figure 25. All cooking. including that of human flesh from diseased 
kinsmen. was done in pits with steam made by pouring water over the hot stones, 
or cooked in bamboo cylinders in the hot ashes. Children participated in both 
the butchery and the handling of cooked meat, rubbing their soiled hands in 
their armpits or hair, and elsewhere on their bodies. They rarely or never 
washed. Infection with the kuru virus was most probably through the cuts and 
abrasions of the skin. or from nose-picking, rye (eye...tss) rubbing, or mucosal 
injury.
These detailed descriptions will be published elsewhere but have reaffirmed 
the oral histories of endocannibalism in the Fore recorded previously12,22–24 
and that this practice ceased abruptly at the time of Australian administrative 
control over the kuru areas. Although isolated events might have occurred for a 
few years after this prohibition, we are confident that new exposures of 
individuals to kuru at mortuary feasts would not have occurred after 1960. Not 
only have no cases of kuru been recorded in people born after 1959 (and only 
nine were recorded in those born after 1956); but also all the 11 last recorded 
cases of kuru that we report here were born before 1950. If any source of 
infection remained, whether from surreptitious cannibalism, possible ground 
contam-ination with human prions at sites where food was prepared, or other 
lateral routes, we would expect individuals born after this period to have 
kuru—especially since children are thought to have had shorter incubation 
periods than adults. However, no such cases have been observed. Additionally, 
although a fraction of hamster-adapted scrapie prions have been shown to survive 
in soil for at least 3 years,25 the mortuary feast practices (during which the 
entire body would be consumed) were undertaken so that any substantial 
contamination of soil would not have occurred, and traditional bamboo knives and 
leaf plates were burned after the feast. Furthermore, no clusters of kuru cases, 
as seen earlier in the epidemic,26 have been recorded for many years.... http://kuru-tse.blogspot.com/2008/08/conference-celebrating-end-of-kuru-50.html 
Kuru: The Science and the Sorcery 
Special Jury Prize Winner, Pacific International Documentary Film Festival 
2011.
This is the true story of one of the most incredible and challenging 
medical detective stories of the 20th Century; a history of human tragedy, 
adventure and discovery. It is the story of the Fore, a Papuan community 
immersed in cannibalistic mortuary practices and sorcery in one of the most 
remote regions on the planet, and the tragic disease that threatened to wipe out 
their entire population. 
In 1961, a young Australian medical researcher, Michael Alpers, puts up his 
hand to work on a new and strange disease in the Eastern Highlands of Papua New 
Guinea. There, he teams up with an American outer, Dr Carleton Gajdusek, who has 
been in the local Fore region since 1957. For Michael it is the beginning of a 
lifelong obsession.
Together, they are amidst a major epidemic. It is killing over 200 people a 
year with devastating effects. It mainly targets women and children. The local 
people, the Fore, call the disease kuru, their word for shivering. They believe 
it is caused by sorcery.
Michael and Carleton are baffled by the disease. There are no scientific 
disciplines to guide them as they attempt to unravel its mysteries. By pure 
chance, a link is made to a strange transmissible animal disease in sheep, 
Scrapie. The two kuru researchers embark on a 10-year experiment to see if the 
fatal degenerative brain disease in humans could be transmissible like 
Scrapie.
The decision is made to perform an autopsy on a kuru victim and inoculate 
the kuru material into a chimpanzee. Kigea, ayoung girl in the village is 
identified as being in the early stages of kuru. Kigea’s family, gives Michael 
permission to perform an autopsy upon her death.
A brain sample taken from Kigea after her death is flown to the USA and 
injected into a chimpanzee called Daisy. While Michael follows the progress of 
the transmission experiment, he starts to collate all the recorded data on kuru 
and begins to suspect cannibalism as the cause of the spreadof the 
disease.
Within two years, he diagnoses Daisy with kuru. This is a defining moment. 
It confirms kuru is transmissible and can cross the species barrier. The 
revelation, together with epidemiological data collated with anthropologist 
Shirley Lindenbaum, links the Fore’s mortuary feasts (consumption of dead 
relatives) to the transmission of kuru. Cannibalism is the cause, and its origin 
is linked to a rare disease called Creutzfeldt Jakob Disease(CJD), but the story 
of kuru is far from over.
The infecting agent is the first new pathogen – prions – to be discovered 
in over 100 years. Research results in two Nobel prizes: it’s discoveries 
turning scientific understanding upside down, causing rifts in the beliefs ofthe 
science community.
Then Mad Cow Disease (Bovine Spongiform Encephalopathy or BSE) reared its 
head in the mid 1980s, and 10 years later the human variant CJD. All eyes turned 
to kuru, the only model of a prion epidemic in human populations. Many unknowns 
still surround prion diseases: there is no cure for kuru, or any of the prion 
diseases. The effects are devastating and unprecedented incubation periods can 
extend beyond 50 years.
Michael is the key and heart to this story, providing unique access to the 
Fore people, and the world’s other leading authorities on the matter; including 
Americans Prof. DC Gajdusek (Nobel Prize 1976), Prof. Stan Prusiner (Nobel Prize 
1997), Prof Shirley Lindenbaum (Anthropologist) and British Prof. John Collinge 
(Director, MRC Prion Unit, UK). 
Kuru: The Science and the Sorcery combines history, science and 
anthropology to tell a unique and ongoing ‘history of science’ documentary 
spanning five decades. It intertwines the thinking of great minds, locally and 
internationally, to reveal how this rare disease in the remote highlands of PNG 
exploded to international attention and how Prion research has now revealed we 
are all descendants of a remote past of cannibal practices. 
Kuru: The Science and the Sorcery Australian scientist Michael Alpers 
dedicated over 50 years to researching Kuru, an obscure and incurable brain 
disease unique to the Fore people of New Guinea. Kuru was once thought to be a 
psychosomatic illness, an infection, a genetic disorder, even a sorcerer's 
curse, but Alpers' findings pointed to cannibalism as the culprit. Yet a recent 
discovery has proven to be even more disturbing: the malady is linked to mad cow 
disease and its human equivalent, variant CJD. With a decades-long incubation 
period, could a larger outbreak be on its way? 
human flesh taste very sweet
KURU EPIDEMIOLOGICAL PATROLS 
Michael Alpers
First Reports
People of the Kuru region part 1
boy playing with animal bladder, blowing it up like a balloon. ...
People of the Kuru region part 2 
Monday, November 19, 2012 
Prion in Saliva of Bovine Spongiform Encephalopathy–Infected Cattle 
kind regards, terry 
============end...tss============== 
*** Saturday, November 2, 2013 ***
Exploring the risks of a putative transmission of BSE to new species
Wednesday, September 25, 2013 
Presence of subclinical infection in gene-targeted human prion protein 
transgenic mice exposed to atypical BSE 
Wednesday, October 30, 2013 
SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13 
10/30/13 
Monday, August 26, 2013 
The Presence of Disease-Associated Prion Protein in Skeletal Muscle of 
Cattle Infected with Classical Bovine Spongiform Encephalopathy 
Tuesday, September 24, 2013 
NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow 
TSE prion Contamination Suit Cethrin(R) 
*** Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 
Page 1 of 15 ***
Tuesday, July 2, 2013 
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals 
Eliminating ALL remaining BSE barriers to export market
Saturday, November 2, 2013 
APHIS Finalizes Bovine Import Regulations in Line with International Animal 
Health Standards while enhancing the spread of BSE TSE prion mad cow type 
disease around the Globe 
*** The discovery of previously unrecognized prion diseases in both humans 
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of 
prion diseases might be wider than expected and raises crucial questions about 
the epidemiology and strain properties of these new forms. We are investigating 
this latter issue by molecular and biological comparison of VPSPr, GSS and 
Nor98. 
Saturday, July 6, 2013 
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human 
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive 
Prionopathy 
Research Article 
Wednesday, October 09, 2013 
WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 
in compensation REVISED
Thursday, October 10, 2013 
CJD REPORT 1994 increased risk for consumption of veal and venison and lamb 
Monday, October 14, 2013 
Researchers estimate one in 2,000 people in the UK carry variant CJD 
proteins 
Friday, August 16, 2013 
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and 
Contaminated blood products induce a highly atypical prion disease devoid of 
PrPres in primates 
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and 
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all 
it’s sub-types $$$ 
Sunday, August 11, 2013 
Creutzfeldt-Jakob Disease CJD cases rising North America updated report 
August 2013 
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada 
seeing an extreme increase of 48% between 2008 and 2010 
Sunday, October 13, 2013 
CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Sunday, September 08, 2013 
Iatrogenic Creutzfeldt-Jakob disease via surgical instruments and 
decontamination possibilities for the TSE prion 
Thursday, September 26, 2013 
Minimise transmission risk of CJD and vCJD in healthcare settings Guidance 
Sunday, June 9, 2013 
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory 
Committee Meeting Webcast 
Tuesday, May 28, 2013 
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a 
methodological outline for evidence-based guidance 
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 ***
Tuesday, March 05, 2013 
A closer look at prion strains Characterization and important implications 
Prion 
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
TSS

 
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