However, like catastrophic anthorpogenic climate change (CACC), those who believe that a consensus is the same as science (and whose salaries depend on persuading the politicos that, in the face of all the evidence, the consensus is correct) have been shutting down funding to, and ostracising, those who disagree. For those that are interested, I have reposted my article of April 12 2007 below.
Prion for your thoughts
Whilst Fabian Tassano rails—quite correctly—against the Marxist bias in many (if not all) universities, and politicians use the climate change orthodoxy to justify yet more tax rises, it is perhaps a salutory time to emphasise the danger in dogma.
One of very first essays that your humble Devil wrote for his—prematurely aborted—microbiology degree was on the subject of BSE and, of course, CJD. Both of these are in a group of diseases, that also includes scrapie, known as transmissible spongiform encephalopathies (TSEs).
It was research into these TSEs that threw up the concept of the prion, a protein that effectively acted as an infectious agent, for these conditions, in a way that no one had previously thought possible. For various reasons, these prions acted utterly unlike any other protein described: they were, for instance, able to infect cross-species (e.g. from cow to human) as well as survive unprecedented rigours of heat and intestinal digestion whilst retaining both their form and virulence.
At the time that I wrote the essay, I considered prions to be a deeply dubious idea and I remained convinced that they were only a symptom of the disease. My chemical and biological learning—including my Biology A Level experimental project, which involved the investigation (and poisoning with heavy metals, etc.) of various proteins—led me to conclude that the prion concept was absolute bollocks and that there must, therefore, be another transmissive agent. Unfortunately, my microbiology tutor disagreed and refused to mark the piece (although she did acknowledge that it was written well, if in a somewhat flippant style).
Flicking through an old edition of New Scientist—the February 17 2007 issue—I see that, finally, some people in the scientific community are coming around to my way of thinking.
VIRUSES, not prions, may be at the root of diseases such as scrapie, BSE and vCJD.
The widely accepted theory of what causes these so-called "transmissible spongiform encephalopathies" (TSEs), such as mad cow disease, is that deformed proteins called prions corrupt other brain proteins, eventually clogging and destroying brain cells. But this theory has never been proved completely.
Or, if we are being truthful, at all; however, that hasn't stopped a great many scientists making Doomsday proclamations with an ever-increasing desperation in order to secure vast amounts of public money.
Laura Manuelidis of Yale University has insisted for years that virus-like particles observed in TSE-infected brains may be the culprits, but since such brains are degenerating, the particles have been dismissed as general debris.
However, when Manuelidis studied the particles in cultures of neural cells infected with two particular strains of scrapie and CJD, she found they contained particles that had clustered in regular arrays, as viruses do in cells - and no apparent prions (Proceedings of the National Academy of Sciences, vol 104, p 1965). Cells with more particles were better at infecting other cell cultures, while boosting prions did not appear to increase their infectiousness or particle numbers. Agents that disrupt viruses stopped the cells infecting other cultures.
Generally speaking, if it looks like a virus, acts like a virus and
Needless to say, those with a vested interest really are not happy with this idea at all. [Emphasis mine.]
However, leading prion researcher Adriano Aguzzi of the University Hospital of Zurich in Switzerland says Manuelidis won't prove her case without isolating the proposed virus and showing it causes TSE. She should also test other strains for these particles and see if her infected cultures cause TSE in animals, he says.
Despite Aguzzi's challenge, what Manuelidis has found tallies nicely, not only with my own opinion but also with observed practice: I have no doubt that she will obtain the proof that is needed. For, whilst we should beware of basing ideas merely on what we already know, in science—as in almost every other field of endeavour—we should hold true to the principle of Occam's Razor.
So, what is the least complex interpretation—that the transmissive agent is of a type that we already know, or that we should attempt to explain a hitherto unthought-of (and, indeed, observation-defying) group of complex structures? If we combine Occam's Razor with what we know of all other proteins, the prion-as-pathogen theory has never been credible to anyone with a wider knowledge of proteins or of infective agents.
Scandalously—and despite the consistent non-fulfillment of the dire death toll predictions, and the lack of success in replicating the infection path—this has not stopped the prion theory becoming the "consensus" amongst politicians and scientists either too ignorant to know or too greedy to care.
Now that we have found evidence for a tenable, and logical, hypothesis for transmission, it is my hope that we may see some sensible theories brought to light in the TSE debate.
One can only hope that something similar happens to the climate change "concensus"—a dogma which has far more potential for damage to both our prosperity and our personal liberty—before this stupidity causes the sort of death toll that has utterly failed to materialise under the prion orthodoxy.
(Cross-posted [...] at Nourishing Obcurity.)
UPDATE: the day after writing this post, I contacted Laura Manuelidis and she promptly sent me large amounts of her research—including a paper that had been published in The Journal of Cellular Biochemistry 9999:1–19 (2006). It took me some time (and all of the microbiology that I could remember from my degree years) to plough through the technical papers, but I remain convinced that what Dr Manuelidis has found is, indeed, a viral transmission vector for TSEs.
A biography of Laura Manuelidis also led me to a website with some papers hosted as downloadable PDFs, along with the summaries and availability of others.
Sklaviadis TK, Manuelidis L, Manuelidis EE.: Physical properties of the Creutzfeldt-Jakob disease agent. J Virol. 1989, 63:1212-22.
PMID: 2492609 [PubMed - Free in PMC]
The first evidence for an infectious particle with a well-defined viral size and density.
Sklaviadis T, Dreyer R, Manuelidis L.: Analysis of Creutzfeldt-Jakob disease infectious fractions by gel permeation chromatography and sedimentation field flow fractionation. Virus Res. 1992, 26:241-54.
PMID: 1492497 [PubMed - Reprint available on request]
This paper shows with the then newly developed technique of field flow fractionation that more purified infectious particles in CJD band with 30nm diameter spheres. It also reports dense EM particles of the same diameter in infectious fractions.
Manuelidis L, Sklaviadis T, Akowitz A, Fritch W.: Viral particles are required for infection in neurodegenerative Creutzfeldt-Jakob disease. Proc Natl Acad Sci U S A. 1995; 92:5124-8.
PMID: 7761460 [PubMed - Free in PMC]
This paper shows that when the 25-30nm viruslike particles are disrupted so that their nucleic acids are dissociated from protective proteins, their infectivity is lost.
Evolution of a strain of CJD that induces BSE-like plaques. Science. 1997;277:94-8.
PMID: 9204907 [PubMed – Free at Science]
This paper shows that a sporadic CJD strain can evolve into one that produces plaques, as in vCJD. This evolution implies there is a mutable nucleic acid genome that defines each TSE strain.
This is incredibly important work but, other than the New Scientist article mentioned above, I have never seen another word of this discovery mentioned (although I only follow this stuff as a hobby these days).