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Manganese enhances prion protein survival in model soils and increases prion infectivity to cells


Reference:

Davies, P. and Brown, D. R., 2009. Manganese enhances prion protein survival in model soils and increases prion infectivity to cells. PLoS ONE, 4 (10), e7518.

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    Official URL:

    http://dx.doi.org/10.1371/journal.pone.0007518

    Abstract

    Prion diseases are considered to be transmissible. The existence of sporadic forms of prion diseases such as scrapie implies an environmental source for the infectious agent. This would suggest that under certain conditions the prion protein, the accepted agent of transmission, can survive in the environment. We have developed a novel technique to extract the prion protein from soil matrices. Previous studies have suggested that environmental manganese is a possible risk factor for prion diseases. We have shown that exposure to manganese is a soil matrix causes a dramatic increase in prion protein survival (similar to 10 fold) over a two year period. We have also shown that manganese increases infectivity of mouse passaged scrapie to culture cells by 2 logs. These results clearly verify that manganese is a risk factor for both the survival of the infectious agent in the environment and its transmissibility.

    Details

    Item Type Articles
    CreatorsDavies, P.and Brown, D. R.
    DOI10.1371/journal.pone.0007518
    DepartmentsFaculty of Science > Biology & Biochemistry
    Publisher Statementjournal.pone.0007518.pdf: © 2009 Davies, Brown. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Davies P, Brown DR (2009) Manganese Enhances Prion Protein Survival in Model Soils and Increases Prion Infectivity to Cells. PLoS ONE 4(10): e7518. http://dx.doi.org/10.1371/journal.pone.0007518
    RefereedYes
    StatusPublished
    ID Code17548
    Additional InformationThis research was supported by funding from the European Commission Quality of Life 5th Framework Programme (QLRT - 2001 - 02723) and studentship (Paul Davies) from the Biotechnology and Biological Sciences Research Council (BBSRC) of the UK. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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