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