Replication of the scrapie agent in hamsters infected intracerebrally confirms the pathogenesis of an amyloid-inducing virosis.
Following intracerebral infection of hamsters with scrapie agent replication started with or without a very short lag phase. Infectivity titres increased exponentially within 35 to 40 days post-infection to a maximum level of 3 x 10(9) LD50 per brain and then remained constant until death. Minimal detectable amounts of scrapie-associated fibrils (SAF) appeared at 42 days and reached high levels 56 days after inoculation. The first clinical symptoms were diagnosed at about 65 days and animals died after 85 to 95 days. These data confirm earlier results in which peripheral infection first revealed agent replication, then SAF formation and finally clinical disease. Unconventional virus diseases, therefore, can best be described as virus-induced, organ-specific amyloidoses.
D000686:Amyloidosis / Q000209:etiology*; D000818:Animals; D006224:Cricetinae; D008647:Mesocricetus; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D018622:PrP 27-30 Protein; D011328:Prions / Q000472:pathogenicity / Q000502:physiology*; D012608:Scrapie / Q000150:complications* / Q000473:pathology; D014779:Virus Replication
D009419:Nerve Tissue Proteins; D011328:Prions; D018622:PrP 27-30 Protein