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CJD and Scrapie Require Agent-Associated Nucleic Acids for Infection.‏

Discussion in 'Other Health News and Research' started by lansbergen, Feb 1, 2016.

  1. lansbergen

    lansbergen Senior Member

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    CJD and Scrapie Require Agent-Associated Nucleic Acids for Infection.
    http://www.ncbi.nlm.nih.gov/pubmed/26773845Abstract

    Unlike Alzheimer's and other neurodegenerative diseases, Transmissible Spongiform Encephalopathies (TSEs) are all caused by actively replicating infectious particles of viral size and density. Different strain-specific TSE agents cause CJD, kuru, scrapie, and BSE, and all behave as latent viruses that evade adaptive immune responses and can persist for years in lymphoreticular tissues. A foreign viral structure with a nucleic acid genome best explains these TSE strains and their endemic and epidemic spread in susceptible species. Nevertheless, it is widely believed that host prion protein (PrP), without any genetic material, encodes all these strains. We developed rapid infectivity assays that allowed us to reproducibly isolate infectious particles where >85% of the starting titer separated from the majority of host components, including PrP. Remarkably, digestion of all forms of PrP did not reduce brain particle titers. To ask if TSE agents, as other viruses, require nucleic acids, we exposed high titer FU-CJD and 22L scrapie particles to potent nucleases. Both agent-strains were propagated in GT1 neuronal cells to avoid interference by complex degenerative brain changes that can impede nuclease digestions. After exposure to nucleases that are active in sarkosyl, infectivity of both agents was reproducibly reduced by >99%. No gold-stained host proteins or any form of PrP were visibly altered by these nucleases. In contrast, co-purifying protected mitochondrial DNA and circular SPHINX DNAs were destroyed. These findings demonstrate that TSE agents require protected genetic material to infect their hosts, and should open reinvestigation of essential agent nucleic acids. This article is protected by copyright. All rights reserved.
     
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  2. JohnCB

    JohnCB Immoderate

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    I take it that this research is rebutting the claim back at the time of the BSE crisis that these diseases were transmitted by protein assemblies alone. I recall that some were saying that some proteins had folded incorrectly and this type of error was transmitted by the protein alone. I had trouble getting my head around that idea. I guess new techniques allow new findings. Is this new work saying that there is some sort of newly discovered virus that is causing and transmitting these diseases?
     
  3. lansbergen

    lansbergen Senior Member

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    Science evolves and what was the holy grail has got cracks. I never was impressed by the arguments used by the protein only fanatics.

    I do not doubt the different folded protein is part of the disease process but I never believed the protein only. hypothese. Prof Laura Manuelidis who was working on these agents before the protein only hypothese was launced, kept working to find the true nature of these agents,

    Nowadays Prpsc usely is called a surrogate marker
     

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