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From: TSS (216-119-143-136.ipset23.wt.net)
Subject: Subclinical Bovine Spongiform Encephalopathy Infection in Transgenic Mice Expressing Porcine Prion Protein
Date: January 1, 2005 at 7:21 am PST

-------- Original Message --------
Subject: Subclinical Bovine Spongiform Encephalopathy Infection in Transgenic Mice Expressing Porcine Prion Protein
Date: Sat, 1 Jan 2005 09:19:30 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


##################### Bovine Spongiform Encephalopathy #####################

Neurobiology of Disease
Subclinical Bovine Spongiform Encephalopathy Infection in Transgenic
Mice Expressing Porcine Prion Protein

Joaquín Castilla,1 Alfonso Gutiérrez-Adán,2 Alejandro Brun,1 Deirdre
Doyle,3 Belén Pintado,2 Miguel A. Ramírez,2 Francisco J. Salguero,1
Beatriz Parra,1 Fayna Díaz San Segundo,1 José M. Sánchez-Vizcaíno,1 Mark
Rogers,3 and Juan M. Torres1

1Centro de Investigación en Sanidad Animal, Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, Valdeolmos, 28130
Madrid, Spain, 2Departamento de Reproducción Animal y Conservación de
Recursos Zoogenéticos, 28040 Madrid, Spain, and 3Department of Zoology
and Conway Institute for Biomolecular and Biomedical Research,
University College Dublin, Belfield, Dublin 4, Ireland

The bovine-porcine species barrier to bovine spongiform encephalopathy
(BSE) infection was explored by generating transgenic mouse lines
expressing the porcine prion protein (PrP) gene. All of the porcine
transgenic (poTg) mice showed clinical signs of BSE after intracerebral
inoculation with a high-titer BSE inoculum. The protease-resistant PrP
(PrPres) was detected in 14% (3 of 22) of the BSE-infected poTg mice by
immunohistochemical or immunoblot analysis. Despite being able to infect
42% (5 of 12) of control mice, a low-dose BSE inoculum failed to
penetrate the species barrier in our poTg mouse model. The findings of
these infectivity studies suggest that there is a strong species barrier
between cows and pigs. However, after second-passage infection of poTg
mice using brain homogenates of BSE-inoculated mice scoring negative for
the incoming prion protein as inoculum, it was possible to detect the
presence of the infectious agent. Thus, porcine-adapted BSE inocula were
efficient at infecting poTg mice, giving rise to an incubation period
substantially reduced from 300 to 177 d after inoculation and to the
presence of PrPres in 100% (21 of 21) of the mice. We were therefore
able to conclude that initial exposure to the bovine prion may lead to
subclinical infection such that brain homogenates from poTg mice
classified as uninfected on the basis of the absence of PrPres are
infectious when used to reinoculate poTg mice. Collectively, our
findings suggest that these poTg mice could be used as a sensitive
bioassay model for prion detection in pigs.

Key words: BSE transmission; porcine prion; PrP; scrapie; transgenic
mice; species barrier

------------------------------------------------------------------------
Received Dec 7, 2003; revised April 7, 2004; accepted April 9, 2004.


http://www.jneurosci.org/cgi/content/abstract/24/21/5063


TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########


Transmission of the BSE Agent to Mice in the Absence of Detectable Abnormal Prion Protein

Corinne I. Lasmézas, * Jean-Philippe Deslys, Olivier Robain, Alexandre Jaegly, Vincent Beringue, Jean-Michel Peyrin, Jean-Guy Fournier, Jean-Jacques Hauw, Jean Rossier, Dominique Dormont

The agent responsible for transmissible spongiform encephalopathies (TSEs) is thought to be a malfolded, protease-resistant version (PrPres) of the normal cellular prion protein (PrP). The interspecies transmission of bovine spongiform encephalopathy (BSE) to mice was studied. Although all of the mice injected with homogenate from BSE-infected cattle brain exhibited neurological symptoms and neuronal death, more than 55 percent had no detectable PrPres. During serial passage, PrPres appeared after the agent became adapted to the new host. Thus, PrPres may be involved in species adaptation, but a further unidentified agent may actually transmit BSE.

C. I. Lasmézas, J.-P. Deslys, A. Jaegly, V. Beringue, J.-M. Peyrin, D. Dormont, Commissariat à l'Energie Atomique, Service de Neurovirologie, DSV/DRM/SSA, B.P. 6, 60-68 avenue du General Leclerc, 92265 Fontenay-aux-Roses Cedex, France.
O. Robain, Hôpital Saint Vincent de Paul, INSERM U 29, 74 avenue Denfert-Rochereau, 75674 Paris Cedex 14, France.
J.-G. Fournier, Hôpital de la Salpétrière, INSERM U 153, 47 boulevard de l'Hôpital, 75651 Paris Cedex 13, France.
J.-J. Hauw, Hôpital de la Salpétrière, Laboratoire Escourolle, INSERM U 360, 47 boulevard de l'Hôpital, 75651 Paris Cedex 13, France.
J. Rossier, Ecole Supérieure de Physique et Chimie Industrielles, CNRS URA 2054, 10 rue Vauquelin, 75231 Paris Cedex 5, France.
* To whom correspondence should be addressed. E-mail: CORINNE.LASMEZAS@cea.fr

http://www.sciencemag.org/cgi/content/abstract/275/5298/402

TSS




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