The new variant of Creutzfeldt-Jakob disease (CJD), which is probably
due to the same agent as bovine spongiform encephalopathy, and kuru is
probably due to an infectious agent absorbed via the digestive tract.
Experimentally, the prion protein PrPSc multiplies in the reticuloend
othelial system of the spleen; it may cross the liver, or even multipl
y in Kuppfer cells, before penetrating into the brain. When injected i
nto the brain of animals, liver specimens from patients who died of CJ
D can induce spongiform encephalopathy, even if they do not contain de
tectable prions. Hepatic laboratory test and histologic abnormalities
have also been reported in prion-associated diseases. They deserve att
ention, although they have not yet been well studied.