Bluestem":hybthx1w said:
I don't like reading about this stuff. But think its important to keep up with it. Here's a link=
http://www.sciencedaily.com/releases/20 ... 144506.htm
amen! :clap:
J. Biol. Chem., Vol. 282, Issue 49, 35878-35886, December 7, 2007
High Titers of Transmissible Spongiform Encephalopathy Infectivity
Associated with Extremely Low Levels of PrPSc in Vivo*
Rona M. Barron12, Susan L. Campbell13, Declan King, Anne Bellon, Karen E.
Chapman¶, R. Anthony Williamson, and Jean C. Manson
From the Neuropathogenesis Unit, Roslin Institute, Ogston Building, West
Mains Road, Edinburgh EH9 3JF, Scotland, United Kingdom, the Department of
Immunology, Scripps Research Institute, La Jolla, California 92037, and the
¶Centre for Cardiovascular Sciences, Queen's Medical Research Institute,
University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ,
Scotland, United Kingdom
Diagnosis of transmissible spongiform encephalopathy (TSE) disease in humans
and ruminants relies on the detection in post-mortem brain tissue of the
protease-resistant form of the host glycoprotein PrP. The presence of this
abnormal isoform (PrPSc) in tissues is taken as indicative of the presence
of TSE infectivity. Here we demonstrate conclusively that high titers of TSE
infectivity can be present in brain tissue of animals that show clinical and
vacuolar signs of TSE disease but contain low or undetectable levels of
PrPSc. This work questions the correlation between PrPSc level and the titer
of infectivity and shows that tissues containing little or no proteinase
K-resistant PrP can be infectious and harbor high titers of TSE infectivity.
Reliance on protease-resistant PrPSc as a sole measure of infectivity may
therefore in some instances significantly underestimate biological
properties of diagnostic samples, thereby undermining efforts to contain and
eradicate TSEs.
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Received for publication, May 25, 2007 , and in revised form, September 24,
2007.
* This work was supported by United Kingdom Department for Environment,
Food, and Rural Affairs Grant SE1437. The costs of publication of this
article were defrayed in part by the payment of page charges. This article
must therefore be hereby marked "advertisement" in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact.
The on-line version of this article (available at
http://www.jbc.org)
contains supplemental Figs. S1–S3 and Table S1.
1 Both authors contributed equally to this work.
3 Current address: Medical Research Council Clinical Sciences Centre,
Imperial College, Hammersmith Campus, Du Cane Road, London W12 0NN, United
Kingdom.
2 To whom correspondence should be addressed. Tel.: 44-131-667-5204; Fax:
44-131-668-3872; E-mail:
[email protected].
http://www.jbc.org/cgi/content/abstract ... type=HWCIT
Volume 13, Number 12–December 2007
Research
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and
Richard A. Bessenâ€
*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and
†Montana State University, Bozeman, Montana, USA
Abstract
Transmissible mink encepholapathy (TME) is a foodborne transmissible
spongiform encephalopathy (TSE) of ranch-raised mink; infection with a
ruminant TSE has been proposed as the cause, but the precise origin of TME
is unknown. To compare the phenotypes of each TSE, bovine-passaged TME
isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents
(typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine
transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to
infection with bovine-passaged TME, typical BSE, and L-type BSE but not to
H-type BSE. Based on survival periods, brain lesions profiles,
disease-associated prion protein brain distribution, and biochemical
properties of protease-resistant prion protein, typical BSE had a distint
phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.
The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4
mice suggest that L-type BSE is a much more likely candidate for the origin
of TME than is typical BSE.
snip...
Conclusion
These studies provide experimental evidence that the Stetsonville TME agent
is distinct from typical BSE but has phenotypic similarities to L-type BSE
in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely
candidate for a bovine source of TME infection than typical BSE. In the
scenario that a ruminant TSE is the source for TME infection in mink, this
would be a second example of transmission of a TSE from ruminants to
non-ruminants under natural conditions or farming practices in addition to
transmission of typical BSE to humans, domestic cats, and exotic zoo animals
(37). The potential importance of this finding is relevant to L-type BSE,
which based on experimental transmission into humanized PrP transgenic mice
and macaques, suggests that L-type BSE is more pathogenic for humans than
typical BSE (24,38).
http://www.cdc.gov/eid/content/13/12/18 ... =eid1887_e
SEE FULL TEXT TME
http://transmissible-mink-encephalopathy.blogspot.com/
TSS
