Free Radicals - Michael Brooks [37]
The fact that no one had found any nucleic acids associated with the infectious agent didn’t mean that they weren’t there. In 1982, shortly after Science published Prusiner’s paper, Richard Kimberlin of the Animal Research Centre in Edinburgh countered it in Nature. It was entirely possible, he said, that the infectious agent was an information-carrying molecule, the ‘virino’, most probably made of nucleic acid but contained in a protein coating. Whereas a virus encodes the instructions for making its proteins and nucleic acids, a virino would encode only the instructions to make the nucleic acids. The genome of the host organism would specify what proteins would be made in the event of infection.
The supporters of the virino hypothesis were – and still are – keen to point out that this would explain the slightly different forms these diseases take in different organisms. The prion hypothesis has yet to explain how these different ‘strains’ develop. The prion supporters argue back that, like the prion, the virino has never been found. What’s more, a virino would be destroyed by enzymes or radiation blasts, while the infectious agent for scrapie and the other diseases emerges unharmed from such attacks. Aha, say the virino people, we know of plenty of viruses that can survive enzyme or radiation attack.
And so it goes on. There are all kinds of subtleties in the diseases that neither camp’s hypothesis can explain. The evidence, such as it is, does not yet allow us to choose between them. And that is why Prusiner’s 1997 Nobel Prize caused such a stink.
After the Nobel Prize announcement, members of the Karolinska Institute, the committee that decides on the recipients, found themselves in the awkward position of having to defend their choice. Lars Edström, for example, acknowledged that there were people who don’t believe that a protein can cause the family of diseases that includes kuru, scrapie and CJD. ‘But we believe it,’ he told the New York Times. ‘From our point of view, there is no doubt.’
Many scientists immediately expressed outrage that the Nobel Prize committee was invoking faith, not facts. Bruce Chesebro, who led the research effort into the causes of scrapie, kuru, BSE and related diseases at the Rocky Mountain Laboratory, issued a press release outlining his objections. ‘No one knows what a “prion” really is,’ he pointed out. If the award of the Nobel stopped people looking for a virus, he said, the result could be ‘tragic’. Laura Manuelidis made a similar point: she told the New York Times of her fears that debate would now be stifled. In the same article, Robert Rohwer, a research director at the Veterans Affairs Medical Center in Baltimore, went further and compared prion science to the cold fusion debacle that had rocked physics in 1989, when two researchers caused an enormous stir by claiming to have created energy-releasing nuclear reactions at room temperature. No one has ever managed to replicate that result, and the physicists in question lost their careers over the issue. In Science, Rohwer called Prusiner’s prion hypothesis ‘the cold fusion of infectious disease’. In other words, it might be radical and appealing, but it is entirely unproven.
A few months after the announcement, Chesebro repeated his appeal for prions to be taken with a pinch of salt. This time it was in a paper in Science that outlined the reasons why the Nobel committee’s award for the prion hypothesis should not be closing the book on diseases such as scrapie and CJD. ‘Clearly, we are in the very early