J Gen Virol
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Published online ahead of print on 17 June 2009 as doi:10.1099/vir.0.010801-0
Journal of General Virology 2009;90:2563.

A more recent version of this article appeared on October 1, 2009 Originally published as JGV in Press, 10.1099/vir.0.010801-0 on June 17, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.010801-0
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PrPTSE in muscle-associated lymphatic tissue during the preclinical stage of mice orally-infected with BSE

Franco Cardone1,5, Achim Thomzig2, Walter J Schulz-Schaeffer3, Angelina Valanzano1, Marco Sbriccoli1, Hanin Abdel-Haq1, Silvia Graziano1, Sandra Pritzkow2, Maria Puopolo1, Paul Brown4, Michael Beekes2 and Maurizio Pocchiari1

1 Istituto Superiore di Sanità;
2 Robert Koch-Institut, Berlin, Germany;
3 Georg-August University, Goettingen, Germany;
4 None

* Corresponding author; email: franco.cardone{at}iss.it

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

Received 4 February 2009; accepted 17 June 2009.




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