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Volume 26, Number 6—June 2020

Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice

Alba Marín-Moreno1, Alvina Huor1, Juan Carlos Espinosa, Jean Yves Douet, Patricia Aguilar-Calvo2, Naima Aron, Juan Píquer, Sévérine Lugan, Patricia Lorenzo, Cecile Tillier, Hervé Cassard, Olivier Andreoletti, and Juan María TorresComments to Author 
Author affiliations: Centro de Investigación en Sanidad Animal, Madrid, Spain (A. Marín-Moreno, J.C. Espinosa, P. Aguilar-Calvo, J. Píquer, P. Lorenzo, J.M. Torres); Interactions Hôte Agent Pathogène–École Nationale Vétérinaire de Toulouse, Toulouse, France (A. Huor, J.Y. Douet, N. Aron, S. Lugan, C. Tiller, H. Cassard, O. Andreoletti)

Main Article

Table 2

Intracerebral inoculation of TgBo, TgVRQ, and TgARQ mice with atypical BSE isolates to promote adaptation to the sheep-PrP sequence in a study of atypical BSE transmission using isolates from different countries in Europe and transgenic mouse models overexpressing human normal brain prion protein*

Isolate Mean survival time, d + SD (n/n0)†
P1 P2 P1 P2 P1 P2
263 + 31 (6/6)
208 + 21 (6/6)

438 + 20 (6/6)
168 + 22 (6/6)

386‡, 404 (2/6)
155 + 8 (6/6)
BSE H3 382 + 74 (6/6) 262 + 3 (6/6) 801 (1/6) 408 + 44 (6/6) >700 (0/6) >700 (0/6)

*BSE, bovine spongiform encephalopathy; dpi, days post-inoculation; n/n0, diseased proteinase K–resistant prion protein–positive/inoculated animals; P1, first passage; P2, second passage.
†Survival time is indicated as mean dpi + SD for all mice that scored positive for proteinase K–resistant prion protein.
‡Found dead animals without clinical signs and positive for proteinase K–resistant disease-associated isoform.

Main Article

1These first authors contributed equally to this article.

2Current affiliation: University of California–San Diego, La Jolla, California, USA.

Page created: May 18, 2020
Page updated: May 18, 2020
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