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Gareth Craig

gcraig@iol.ie      

 

The Cause?

Over the last few decades many tests have performed on infected brain matter, first from scrapie cases, then cases of BSE, CJD and other recent TSEs, scanning it with every known method for remnants of bacteria, a virus or any other known infective agent; but to no avail. The only tests that showed any consistent differences between samples of diseased and unaffected brain were screenings by gel electrophoresis, first performed by the scientist David Bolton. When the results were developed a thick band was present in the readings for each of the samples of diseased brain, and absent from those of the healthy samples. This signaled the presence of a different form of protein that had to be associated with the disease, and it was always found to be only present in TSE affected brain whenever the procedure was repeated. This protein has since been identified as PrPsc, or the Prion.

When first announced, the idea that a protein could be the sole agent of a disease was viewed as scientific heresy, as it was a cardinal rule of biology that reproduction of any form requires Nucleic Acid (NA) in order for the hereditary characteristics of the species / strain to be handed on; this applied for everything from the grandest mammal to the lowliest virus or bacteria. The protein as put forward contained no form of NA, and yet reproduction was clearly taking place. Steadily though, in the absence of evidence of any other agent, support has steadily grown among the scientific community for the Prion Theory; although there is still no concrete proof whether it is the actual agent of the TSEs, or simply a byproduct of the TSE diseases.

A second, though much more marginal theory is that the agent of TSEs is an organism called a Virino, a smaller version of a virus composed of simple RNA for the genetic information, surrounded by a tough shell of protein.


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The information on this website has not been updated since
March 1997

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