The astonishing recognition that self-propagating changes in protein struct
ure may be at the basis of spongiform encephalopathies is changing our view
s of transmissible diseases. Infectious agents consisting of abnormally fol
ded proteins(i.e., the prion) can propagate in host organisms using previou
sly unrecognized routes and invade the brain after a dangerous liaison with
the immune system. The identification of the nodal points of neuroinvasion
and new techniques to amplify minute amounts of misfolded proteins may ope
n the possibility for post exposure prophylaxis.