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From: TSS ()
Subject: Prion biology relevant to bovine spongiform encephalopathy
Date: June 1, 2005 at 9:19 am PST

Greetings,

This article below ;

J. Novakofski, M. S. Brewer, N. Mateus-Pinilla, J. Killefer, and R. H. McCusker
Prion biology relevant to bovine spongiform encephalopathy
J Anim Sci, June 1, 2005; 83(6): 1455 - 1476.


SPECIAL TOPICS
Prion biology relevant to bovine spongiform encephalopathy1
J. Novakofski*,2, M. S. Brewer, N. Mateus-Pinilla, J. Killefer* and R. H. McCusker*
* Departments of Animal Sciences and Food Science and Human Nutrition, University of Illinois at Urbana–Champaign 61801-4737; and Illinois Natural History Survey, Center for Wildlife and Plant Ecology, Champaign, IL 61820

2 Correspondence: 1503 South Maryland Dr. (phone: 217-333-6181; e-mail: Jnova@uiuc.edu ).


Bovine spongiform encephalopathy (BSE) and chronic wasting disease (CWD) of deer and elk are a threat to agriculture and natural resources, as well as a human health concern. Both diseases are transmissible spongiform encephalopathies (TSE), or prion diseases, caused by autocatalytic conversion of endogenously encoded prion protein (PrP) to an abnormal, neurotoxic conformation designated PrPsc. Most mammalian species are susceptible to TSE, which, despite a range of species-linked names, is caused by a single highly conserved protein, with no apparent normal function. In the simplest sense, TSE transmission can occur because PrPsc is resistant to both endogenous and environmental proteinases, although many details remain unclear. Questions about the transmission of TSE are central to practical issues such as livestock testing, access to international livestock markets, and wildlife management strategies, as well as intangible issues such as consumer confidence in the safety of the meat supply. The majority of BSE cases seem to have been transmitted by feed containing meat and bone meal from infected animals. In the United Kingdom, there was a dramatic decrease in BSE cases after neural tissue and, later, all ruminant tissues were banned from ruminant feed. However, probably because of heightened awareness and widespread testing, there is growing evidence that new variants of BSE are arising "spontaneously," suggesting ongoing surveillance will continue to find infected animals. Interspecies transmission is inefficient and depends on exposure, sequence homology, TSE donor strain, genetic polymorphism of the host, and architecture of the visceral nerves if exposure is by an oral route. Considering the low probability of interspecies transmission, the low efficiency of oral transmission, and the low prion levels in nonnervous tissues, consumption of conventional animal products represents minimal risk. However, detection of rare events is challenging, and TSE literature is characterized by subsequently unsupported claims of species barriers or absolute tissue safety. This review presents an overview of TSE and summarizes recent research on pathogenesis and transmission.


Key Words: Bovine Spongiform Encephalopathy • Chronic Wasting Disease • Prion

http://www.animal-science.org/cgi/content/abstract/83/6/1455


WAS one sited to ;

Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.


--------------------------------------------------------------------------------

C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: salvatore.monaco@mail.univr.it .
www.pnas.org/cgi/doi/10.1073/pnas.0305777101


This article has been cited by other articles in HighWire Press-hosted journals:

http://www.pnas.org/cgi/content/abstract/0305777101v1

Greetings again,

I had to read it twice to believe what I had read. SO, I thought I might try and comment to the journal and the author of the article. Here is the thread for those who might be interested. Never could get the author to reply ;


----- Original Message -----
From: "Galyean, Michael"
To:
Cc:
Sent: Saturday, May 28, 2005 3:34 PM
Subject: FW: Prion biology relevant to bovine spongiform encephalopathy (ANIMALSCI Feedback Form)


Dr. Novakofski:

I recevied the following message and comments regarding your recent paper on prion biology published in the Journal of Animal Science. I hope you will take the time to look over the comments and respond to Mr. Singeltary.

Regards,

Michael Galyean
Editor-in-Chief
Journal of Animal Science

________________________________

From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Thu 5/26/2005 9:20 AM
To: Amanda Kolling
Cc: Galyean, Michael
Subject: Re: Prion biology relevant to bovine spongiform encephalopathy (ANIMALSCI Feedback Form)


I have forwarded this to Dr. Michael Gaylean as suggested.
thank you........

please note new email address flounder9@verizon.net

any questions or follow ups, please do not hesitate to write...

thank you,

kindest regards,
Terry S. Singeltary Sr.

----- Original Message -----
From: Amanda Kolling
To: Terry S. Singeltary Sr.
Sent: Thursday, May 26, 2005 8:11 AM
Subject: RE: Prion biology relevant to bovine spongiform encephalopathy (ANIMALSCI Feedback Form)


Dear Mr. Singeltary,

Thank you for your comments. Contrary to a previous e-mail sent to you by an employee of HighWire, the Journal of Animal Science does accept Letters to the Editor. If you are interested in submitting this as a letter to the editor, I urge you to contact our editor-in-chief, Dr. Michael Gaylean at michael.galyean@ttu.edu.

Best regards,

Amanda Kolling
Technical Editor,
Journal of Animal Science


At 09:11 AM 5/17/2005 -0700, Terry S. Singeltary Sr. wrote:
>------------------------------------------------------------
>Comments sent via JAS Feedback Page
>------------------------------------------------------------
> NAME: Terry S. Singeltary Sr.
> EMAIL: flounder@wt.net
> IP ADDRESS: 216.119.139.23
> HOSTNAME: pool139-23.dial-p1.hou.wt.net
> PREVIOUS PAGE: http://jas.fass.org/cgi/content/abstract/83/6/1455
> BROWSER: Mozilla/5.0 (Windows; U; Win98; en-US; rv:1.0.2)
> Gecko/20030208 Netscape/7.02
> PROMOTIONAL USE: Granted
>------------------------------------------------------------
>COMMENTS:
>J. Anim. Sci. 2005. 83:1455-1476
>© 2005 American Society of Animal Science
>SPECIAL TOPICS
>Prion biology relevant to bovine spongiform encephalopathy1
>J. Novakofski*,2, M. S. Brewer{dagger}, N.
>Mateus-Pinilla{ddagger}, J. Killefer* and R. H. McCusker*
>
>* Departments of Animal Sciences and {dagger} Food
>Science and Human Nutrition, University of Illinois at
>Urbana­Champaign 61801-4737; and {ddagger} Illinois
>Natural History Survey, Center for Wildlife and Plant
>Ecology, Champaign, IL 61820
>
>2 Correspondence: 1503 South Maryland Dr. (phone:
>217-333-6181; e-mail: Jnova@uiuc.edu).
>
>Bovine spongiform encephalopathy (BSE) and chronic
>wasting disease (CWD) of deer and elk are a threat to
>agriculture and natural resources, as well as a human
>health concern. Both diseases are transmissible
>spongiform encephalopathies (TSE), or prion diseases,
>caused by autocatalytic conversion of endogenously
>encoded prion protein (PrP) to an abnormal, neurotoxic
>conformation designated PrPsc. Most mammalian species
>are susceptible to TSE, which, despite a range of
>species-linked names, is caused by a single highly
>conserved protein, with no apparent normal function. In
>the simplest sense, TSE transmission can occur because
>PrPsc is resistant to both endogenous and environmental
>proteinases, although many details remain unclear.
>Questions about the transmission of TSE are central to
>practical issues such as livestock testing, access to
>international livestock markets, and wildlife
>management strategies, as well as intangible issues
>such as consumer confidence in the safety of the meat
>supply. The majority of BSE cases seem to have been
>transmitted by feed containing meat and bone meal from
>infected animals. In the United Kingdom, there was a
>dramatic decrease in BSE cases after neural tissue and,
>later, all ruminant tissues were banned from ruminant
>feed. However, probably because of heightened awareness
>and widespread testing, there is growing evidence that
>new variants of BSE are arising "spontaneously,"
>suggesting ongoing surveillance will continue to find
>infected animals. Interspecies transmission is
>inefficient and depends on exposure, sequence homology,
>TSE donor strain, genetic polymorphism of the host, and
>architecture of the visceral nerves if exposure is by
>an oral route. Considering the low probability of
>interspecies transmission, the low efficiency of oral
>transmission, and the low prion levels in nonnervous
>tissues, consumption of conventional animal products
>represents minimal risk. However, detection of rare
>events is challenging, and TSE literature is
>characterized by subsequently unsupported claims of
>species barriers or absolute tissue safety. This review
>presents an overview of TSE and summarizes recent
>research on pathogenesis and transmission.
>
>Key Words: Bovine Spongiform Encephalopathy . Chronic
>Wasting Disease . Prion
>
>http://jas.fass.org/cgi/content/abstract/83/6/1455
>
> >there is growing evidence that new variants of BSE are
>arising "spontaneously,"
>
>
>THERE is NO evidence of a 'spontaneous' TSE anywhere that
>is infectious and shows the pathology of any natural TSE.
>if i have missed something, could someone please site this
>science to me please.
>
>
> >Considering the low probability of interspecies
>transmission, the low efficiency of oral transmission,
>and the low prion levels in nonnervous tissues,
>consumption of conventional animal products represents
>minimal risk.
>
>
>I DISAGREE with all of the above. all one has to do is
>read transmission
>studies. scrapie infected sheep and goats, CWD infected
>deer and
>elk (who knows how many strains) and undocumented TSEs
>in the
>USA bovine have been rendered and fed to animals for
>humna/animal
>consumption for decades. it's only a pipe dream that
>none of this
>was infectious. to think of a 'spontaneous' TSE as just
>popping
>up from nowhere, is like believing in Santa Claus. remember
>the USA scrapie research in Mission, Texas. IT did NOT look
>like BSE...
>
>
>1: J Infect Dis 1980 Aug;142(2):205-8
>
> Oral transmission of kuru, Creutzfeldt-Jakob
>disease, and scrapie to nonhuman primates.
>
> Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL,
>Gajdusek DC.
>
> Kuru and Creutzfeldt-Jakob disease of humans and
>scrapie disease of sheep and goats were transmitted to
>squirrel monkeys (Saimiri sciureus) that were exposed
>to the infectious agents only by their nonforced
>consumption of known infectious tissues. The
>asymptomatic incubation period in the one monkey
>exposed to the virus of kuru was 36 months; that in the
>two monkeys exposed to the virus of Creutzfeldt-Jakob
>disease was 23 and 27 months, respectively; and that in
>the two monkeys exposed to the virus of scrapie was 25
>and 32 months, respectively. Careful physical
>examination of the buccal cavities of all of the
>monkeys failed to reveal signs or oral lesions. One
>additional monkey similarly exposed to kuru has
>remained asymptomatic during the 39 months that it has
>been under observation.
>
>PMID: 6997404
>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
>
>
>3. You will recall that the advice provided by
>Professor Smith in
>1993 and by Dr. Gore this month used the sub-population
>of dairy
>farm workers who had had a case of BSE on their farms -
>63,000, which is approximately half the number of dairy
>farm
>workers - as a denominator. If the above sums are
>repeated using
>this denominator population, taking an annual incidence
>in the general
>population of 1 per million the observed rate in this
>sub-population
>is 10 TIMES, and taking an annual incidence of 0.7 per
>million,
>IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than
>that in the general population...
>
>http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf
>
>
>It was, however, performed in the USA in 1979, when it
>was shown that
>cattle inoculated with the scrapie agent endemic in the
>flock of Suffolk
>sheep at the United States Department of Agriculture in
>Mission, Texas,
>developed a TSE quite unlike BSE. 32 <
>
>http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543
>
>The findings of the initial transmission, though not of
>the clinical or
>neurohistological examination, were communicated in
>October 1988 to Dr
>Watson, Director of the CVL, following a visit by Dr
>Wrathall, one of
>the project leaders in the Pathology Department of the
>CVL, to the
>United States Department of Agriculture. 33
>
>
>http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546
>
>
>The results were not published at this point, since the
>attempted
>transmission to mice from the experimental cow brain
>had been
>inconclusive. The results of the clinical and
>histological differences
>between scrapie-affected sheep and cattle were
>published in 1995.
>Similar studies in which cattle were inoculated
>intracerebrally with
>scrapie inocula derived from a number of
>scrapie-affected sheep of
>different breeds and from different States, were
>carried out at the US
>National Animal Disease Centre. 34
>
>
>http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820549
>
>
>The results, published in 1994, showed that this source
>of scrapie
>agent, though pathogenic for cattle, did not produce
>the same clinical
>signs of brain lesions characteristic of BSE.
>
>
>http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm
>
>
>Visit to USA ... info on BSE and Scrapie
>
>
>http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
>
>
>HOUND STUDY
>
>AS implied in the Inset 25 we must not _ASSUME_ that
>transmission of BSE to other species will invariably
>present pathology typical of a scrapie-like disease.
>
>snip...
>
>http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
>
>
>In Confidence - Perceptions of unconventional slow
>virus diseases
>of animals in the USA - APRIL-MAY 1989 - G A H Wells
>
>
>http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
>
>WHY is USA insisting _now_ not to use WB, when on the
>1st _confirmed_
>case Dec. 23, 2003
>USA mad cow, WB was used ???
>
>maybe this is the reason ;
>
>JAPAN BSE # 8 & 9 cow
>
>8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
>No clinical signs WB+, IHC-, HP-
>
>
>9. 4/11/2003 Holstein Steer 13/1/2002
>21 mths No clinical signs WB+, IHC-, HP-
>
>===========
>
>More information on the first 11 Japanese BSE-cases can
>be found on the

>website of the Japanese Embassy in the US:
>
>http://www.us.emb-japan.go.jp/english/html/fafacts/bse/bse.htm
>
>
>IN fact, the new strain of TSE in cattle BaSE, does not
>look like nvCJD in humans, but very similar
>to the sporadic CJD;
>
>
>BASE in cattle in Italy of Identification of a second
>bovine amyloidotic spongiform encephalopathy: Molecular
>similarities with sporadic Creutzfeldt-Jakob disease
>
>http://www.pnas.org/cgi/content/abstract/0305777101v1
>
>
>Adaptation of the bovine spongiform encephalopathy
>agent to primates and comparison with Creutzfeldt-
>Jakob disease: Implications for human health THE
>findings from Corinne Ida Lasmézas*, [dagger] ,
>Jean-Guy Fournier*, Virginie Nouvel*, 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 for French
>iatrogenic growth hormone-linked CJD taken as a control
>is very different from vCJD but is similar to that
>found in one case of sporadic CJD and one sheep scrapie
>isolate;
>
>
>http://www.pnas.org/cgi/content/full/041490898v1
>
>
>Characterization of two distinct prion strains derived
>from bovine spongiform encephalopathy transmissions to
>inbred mice
>
>
> http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471
>
>
>USA BSE GBR III
>
>http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/574/sr03_biohaz02_usa_report_annex_en1.pdf
>
>http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
>
>https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
>
>https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
>
>
>Terry S. Singeltary SR.
>P.O. Box 42
>Bacliff, Texas USA 77518

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

La Vonne Gallo
HighWire Press
1454 Page Mill Road
Palo Alto, CA 94304
fax: 650.725.9335
lgallo@highwire.stanford.edu

~~~~~~~~~~~
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

TSS



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