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J Gen Virol. 2017 Jun;98(6):1563-1569. doi: 10.1099/jgv.0.000803. Epub 2017 Jun 14.

Precision in the design of an experimental study deflects the significance of proteinase-activated receptor 2 expression in scrapie-inoculated mice.

Author information

1
1​Institute of Immunology and Microbiology, First Faculty of Medicine, Charles University, Studnickova 7, Prague 2, 128 00, Czech Republic.
2
2​Department of Pathology and Molecular Medicine, Thomayer Teaching Hospital, Videnska 800, Prague 4, 14059, Czech Republic 3​Department of Pathology, First Faculty of Medicine, Charles University, Studnickova 2, Prague 2, 12800, Czech Republic.

Abstract

Proteinase-activated receptor 2 (PAR2) is suspected to modulate the pathogenesis of various neurodegenerative conditions. We previously described delayed onset of clinical symptoms and prolonged survival of PAR2-deficient mice after intracerebral inoculation with prions. Here we report the results from a refined blinded study that aimed to investigate the effects of PAR2 deletion on scrapie pathogenesis after peripheral infection. This study failed to confirm that PAR2 deficiency impacts on the length of the incubation period, with PAR2-/- and PAR2+/+ littermates developing scrapie at the same time. To clarify the discrepancy between the two observations, we repeated the intracerebral inoculation study while utilizing our refined protocol, which aimed to limit possible sources of experimental bias. The study again failed to confirm the significant effect of PAR2 expression on the course of prion infection. Our report emphasizes and discusses the importance of unbiased experimental design and the selection of proper genetic controls when using genetically altered animal models for prion pathogenesis studies.

PMID:
28613153
DOI:
10.1099/jgv.0.000803
[Indexed for MEDLINE]

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