Abstract:
:Variably protease-sensitive prionopathy (VPSPr), a recently identified and seemingly sporadic human prion disease, is distinct from Creutzfeldt-Jakob disease (CJD) but shares features of Gerstmann-Sträussler-Scheinker disease (GSS). However, contrary to exclusively inherited GSS, no prion protein (PrP) gene variations have been detected in VPSPr, suggesting that VPSPr might be the long-sought sporadic form of GSS. The VPSPr atypical features raised the issue of transmissibility, a prototypical property of prion diseases. We inoculated VPSPr brain homogenate into transgenic mice expressing various levels of human PrP (PrPC). On first passage, 54% of challenged mice showed histopathologic lesions, and 34% harbored abnormal PrP similar to that of VPSPr. Surprisingly, no prion disease was detected on second passage. We concluded that VPSPr is transmissible; thus, it is an authentic prion disease. However, we speculate that normal human PrPC is not an efficient conversion substrate (or mouse brain not a favorable environment) and therefore cannot sustain replication beyond the first passage.
journal_name
Emerg Infect Disjournal_title
Emerging infectious diseasesauthors
Notari S,Xiao X,Espinosa JC,Cohen Y,Qing L,Aguilar-Calvo P,Kofskey D,Cali I,Cracco L,Kong Q,Torres JM,Zou W,Gambetti Pdoi
10.3201/eid2012.140548subject
Has Abstractpub_date
2014-12-01 00:00:00pages
2006-14issue
12eissn
1080-6040issn
1080-6059journal_volume
20pub_type
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