Successive passaging of the scrapie strains, ME7-ha and 139A-ha, generated by the interspecies transmission of mouse-adapted strains into hamsters markedly shortens the incubation times, but maintains their molecular and pathological properties.

As a type of zoonotic disease, prion diseases may be transmitted naturally and experimentally among species. In a previous study, we demonstrated that the mouse-adapted scrapie strains, ME7 (ME7-mo) and 139A (139A-mo), can overcome the species barrier and induce experimental scrapie when inoculated into Golden hamsters and generated 2 new hamster-adapted strains, ME7 (ME7-ha) and 139A (139A-ha). In the present study, in order to assess the infectivity and other molecular and neuropathological properties of the newly formed scrapie agents, ME7-ha and 139A-ha were further intracerebrally inoculated into hamsters. Compared with infection with 1st passage strains, the incubation times and clinical courses of infection with 2nd passage strains were markedly shorter, which were quite comparable with those of the mice infected with their parent mouse strains. The glycosylation patterns of brain PrP(Sc) in the animals infected with the 2nd passage of those 2 strains maintained similar features as those in the animals infected with the 1st passage of those strains, with predominantly diglycosylated PrP(Sc). Neuropathological assays revealed comparable spongiform degeneration and microglia proliferation in the brain tissues from the infected mice and hamsters, but markedly more plaque-like deposits of PrP(Sc) and more severe astrogliosis in the brains of the hamster. These data indicate that the strains, ME7-ha 1st and 139A-ha 1st generated by interspecies infection can passage in the new host hamster and stably maintain their molecular and neuropathological characteristics.