The UK epidemic of BSE: Slow virus or chronic pesticide-initiated modification of the prion protein? Part 2: An epidemiological perspective
Abstract This paper elucidates the flaws in the official hypothesis that bovine spongioform encephalopathy originated from alterations in the way that scrapie-contaminated cattlefeeds were manufactured in the UK. An alternative hypothesis is proposed that cites exposure of the bovine embryo to various specific high-dose lipophilic formulations of organophosphates, such as the high-dose phthalimide containing organophosphate phosmet, (which were applied compulsorily and exclusively in the UK during the 1980s/early 1990s) as the primary trigger that initiated the deformation of prion protein and the onset of the bovine spongioform encephalopathy epidemic. The multi-site binding metabolites of these organophosphates penetrate the fetus, covalently phosphorylating various active sites on fetal prion protein. The extra charged phosphate groups left on aged prion protein blocks both proteases and chaperones from accessing their catalytic/bonding sites, creating the undegradable, misfolded isoform of prion protein, PrPsc. The resulting abnormally phosphorylated PrPsc aggregates to freshly synthesized PrPc, transforming it into same; due to a system of positive feedback invoked by the organophosphate-induced blockage of a proon protein-specific protein kinase. Both the timing, distribution and dynamics of usage of these specific organophosphates correlates with the epidemiology of bovine spongioform encephalopathy as well as accounting for the 23 000 cattle that have developed the disease, yet were born after the 1988 ban on scrapie-contaminated cattlefeed.
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