Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion.

Allen Herbst,Camilo Duque Velásquez,Judd M Aiken,Debbie Mckenzie,Elizabeth Triscott

doi:10.3201/eid2309.161474

Abstract

Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.

Highlights

Mice inoculated with H95+ chronic wasting disease (CWD) prions succumbed to clinical disease at 575 ± 47 or 692 ± 9 days, depending on the H95+ isolate (Table)
Mice inoculated with Wisc-1 or elk CWD or uninfected deer homogenates were euthanized at day 708 after infection with no signs of prion disease
Protease-resistant PrPCWD was present in all mice infected with H95+ prions and was not detected in mice infected with Wisc-1 or CWD2

Summary

Introduction

Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection.

Results

Conclusion