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Scrapie pathogenesis in subclinically infected B-cell-deficient mice.


Frigg, R; Klein, M A; Hegyi, I; Zinkernagel, R M; Aguzzi, A (1999). Scrapie pathogenesis in subclinically infected B-cell-deficient mice. Journal of Virology, 73(11):9584-9588.

Abstract

Prion infections can present without clinical manifestations. B-cell deficiency may be a model for subclinical transmissible spongiform encephalopathy, since it protects mice from disease upon intraperitoneal administration of scrapie prions; however, a proportion of B-cell-deficient mice accumulate protease-resistant prion protein in their brains. Here, we have characterized this subclinical disease. In addition, we have studied the possibility that a neurotoxic factor secreted by B cells may contribute to pathogenesis.

Prion infections can present without clinical manifestations. B-cell deficiency may be a model for subclinical transmissible spongiform encephalopathy, since it protects mice from disease upon intraperitoneal administration of scrapie prions; however, a proportion of B-cell-deficient mice accumulate protease-resistant prion protein in their brains. Here, we have characterized this subclinical disease. In addition, we have studied the possibility that a neurotoxic factor secreted by B cells may contribute to pathogenesis.

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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1 November 1999
Deposited On:11 Feb 2008 12:25
Last Modified:05 Apr 2016 12:20
Publisher:American Society for Microbiology
ISSN:0022-538X
Related URLs:http://jvi.asm.org/cgi/content/full/73/11/9584?view=long&pmid=10516067
PubMed ID:10516067
Permanent URL: http://doi.org/10.5167/uzh-1820

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