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Nobel Laureate Obtains Patents

The 1997 Novel Prize for Physiology or Medicine was awarded to Prof. Stanley B. Prusiner of the University of California at San Francisco for his discovery of a new biological principle of infection caused by a new type of infectious agent called ‘prion’. This has been found to cause maladies commonly known as transmissible spongiform encephalopathies (TSEs) which include ‘mad cow’ disease, scrape in sheep, Creuzfeldt-Jakob disease and Kuru in humans. The inventor has used the term ‘prion’ for proteinaceous infectious particle. In the mid 1980s it was discovered that most mammals have naturally in their cells a gene encoding the prion protein. Normally, the gene gives rise to a harmless form of the protein, but this form sometimes takes a variant shape which is insoluble and is often found in the brains of TSE victims. Prusiner’s theory holds that if some of the insoluble form finds its way into a mammal’s brain, it can encourage the normal form to change into the supposedly insoluble variant. However, some reservations have also been expressed, "The idea that prion protein along prompts TSEs still lack unambiguous proof. Only further experiment will reveal whether the Nobel Assembly was hasty". (Scientific American of January 1998).

A patent search on this subject revealed that Prof. Prusiner was perhaps the first inventer to obtain a US Patent related to prion entitled "Method of Detectign Prion in a Sample and Transgenic Animal Used for the Same" in October 1996; the application for the same was filed in 1994. The invention is directed to artificial prion genes that are made up of elements of the prion genes of a host and test species. When these artificial prion genes are inserted into a transgenic mouse, the resultant mouse becomes susceptible to infection with prions that infect the test species but do not normally infect mice. The transgenic animals are useful for testing the presence of prions in a sample. An exemplary claim of the patent is reproduced below : A transgenic mouse having a genome comprised of PrP transgene rendering the mouse susceptible to infection with prions which infect and cause disease in a human; wherein the PrP transgene is comprised of a native mouse PrP gene that has one or more, but not all, of its codons that differ from a human PrP gene replaced with a corresponding human PrP gene codon; and further wherein said transgenic mouse exhibits symptoms of prion disease within 200 days or less after inoculation with a prion that infects and causes prion disease in humans. It appears that the method of detection using a transgenic mouse was evolved for establishing the theory.

He has recently obtained another patent entitled "Formation and Use of Prion Protein (PRP) Complexes" on May 12, 1998 for which the application was filed in 1995. The patent relates to a method of screening for compounds which inhibits the binding of PrP to a PrP peptide, comprising the steps of :

bull1.jpg (4984 bytes) contacting in-vitro test a compound with a purified naturally occurring first component PrP­ C in the presence of purified second component PrP peptide, wherein said PrP peptide has random coil or a helical confirmation, and wherein the first and second components form a prion protein complex with a PrP characteristic selected from the group consisting of

bull2.jpg (4956 bytes) increased b-sheet content,
bull2.jpg (4956 bytes) diminished aqueous solubility, and
bull2.jpg (4956 bytes) resistance to proteolylic digestion, relative to PrP­ C;

bull1.jpg (4984 bytes) detecting formation of a prion protein complex; by determining

bull2.jpg (4956 bytes) increased b-sheet,
bull2.jpg (4956 bytes) diminished aqueous solubility, or
bull2.jpg (4956 bytes) resistance to proteolytic digestion, relative to PrP­ C and

bull1.jpg (4984 bytes) comparing levels of prion protein complex in the presence of said test compound with levels in the absence of the test compound, wherein reduced levels of said prion protein complex in the presence of said test compound is indicative that said test compound inhibits said binding of PrP­ C to a PrP peptide.

It is interesting to note that another leading scientist Charles Weissmann of the University of Zurich has also obtained a US patent on a related work. 8 Patents have been issued by the US Patent Office in this area since 1996.

The above case of patenting in a frontier area shows that fundamental / basic research can also lead to patentable inventions. In the process of arriving at a conclusive research, basic or otherwise, there would be intermediate findings, big or small, which may be inventive and novel in themselves to qualify for grant of patents and these may also be commercially important in their own way. Thus a scientist or a researcher has got to be alert to spot such inventions and need not wait for the final outcome. It also becomes evident that methods of detection and testing have become patentable in some countries and this shift may possibly be arising out of the complexities and uncertainties in a given knowledge area. Nobel Prize winning inventions are commonly understood to be associated with fundamental knowledge, like Raman Effect, which is considered outside the realm of patents. Are we expecting some changes in the basic thought process?

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