HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: vir.0.010801-0v1 vir.0.010801-0v2 90/10/2563    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Cardone, F. Articles by Pocchiari, M. PubMed PubMed Citation Articles by Cardone, F. Articles by Pocchiari, M. Agricola Articles by Cardone, F. Articles by Pocchiari, M.

PrP^TSE in muscle-associated lymphatic tissue during the preclinical stage of mice infected orally with bovine spongiform encephalopathy

Franco Cardone^1,

Achim Thomzig^2,

¹ Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy
² Robert Koch-Institut (P24 – Transmissible Spongiform Encephalopathies), Nordufer 20, 13353 Berlin, Germany
³ Prion and Dementia Research Unit, Department of Neuropathology, University Medical Center, Georg-August University Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany
⁴ 7815 Exeter Road, Bethesda, MD 20814, USA

Correspondence
Franco Cardone
franco.cardone{at}iss.it

The involvement of muscles in the pathogenesis of transmissible spongiform encephalopathies (TSEs) is irregular and unpredictable. We show that the TSE-specific protein (PrP^TSE) is present in muscles of mice fed with a mouse-adapted strain of bovine spongiform encephalopathy as early as 100 days post-infection, corresponding to about one-third of the incubation period. The proportion of mice with PrP^TSE-positive muscles and the number of muscles involved increased as infection progressed, but never attained more than a limited distribution, even at the clinical stage of disease. The appearance of PrP^TSE in muscles during the preclinical stage of disease was probably due to the haematogenous/lymphatic spread of infectivity from the gastrointestinal tract to lymphatic tissues associated with muscles, whereas in symptomatic animals, the presence of PrP^TSE in the nervous system, in neuromuscular junctions and in muscle fibres suggests a centrifugal spread from the central nervous system, as already observed in other TSE models.

These authors contributed equally to this work.