Scrapie pathogenesis in subclinically infected B-cell-deficient mice

R Frigg, MA Klein, I Hegyi, RM Zinkernagel… - Journal of …, 1999 - Am Soc Microbiol
R Frigg, MA Klein, I Hegyi, RM Zinkernagel, A Aguzzi
Journal of Virology, 1999Am Soc Microbiol
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.
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.
American Society for Microbiology