Collinge J et al. 1996, Molecular analysis of prion strain variation and the aetiology of new variant CJD (Nature 383:685-690, PMID 8878476, doi 10.1038/383685a0)

A 1996 Nature paper from John Collinge's group, with Ironside and Hill among the five authors, that used biochemical typing of the disease-associated prion protein and transmission to mice to argue that new variant CJD is a distinct form of human prion disease whose strain characteristics resemble BSE, which supports BSE as its likely source. It is a foundation paper for molecular strain typing of human prion disease and was followed in 1997 by a paper titled "The same prion strain causes vCJD and BSE". This entry is based on bibliographic records, the abstract-level content and a later review by the same senior author; the paper itself sits behind a login and was not opened. Information only.

Key facts

  • The citation is verified: Collinge J, Sidle KC, Meads J, Ironside J, Hill AF, Nature 1996, volume 383, issue 6602, pages 685-690, DOI 10.1038/383685a0, PMID 8878476.
  • The only listed affiliation is the first author's, the Neurogenetics Unit in the Department of Biochemistry and Molecular Genetics at Imperial College School of Medicine at St Mary's, London; the records list no affiliations for the other four authors.
  • The abstract states that TSE strains differ in physicochemical properties of the disease-associated prion protein, and that these differences persist when the agent is passed to transgenic mice.
  • The abstract reports that new variant CJD has strain characteristics distinct from other CJD types and resembling those of BSE transmitted to mice, domestic cats and macaques, consistent with BSE as the source of the new disease.
  • The abstract also suggests that the prion protein itself may encode disease phenotype.
  • A 2001 review by Jackson and Collinge cites the paper for four points: human and bovine prions passed to wild-type mice give mouse prion protein keeping the fragment sizes and glycoform ratios of the inoculum; vCJD glycoform ratios differ from classic CJD; similar ratios are seen in BSE and BSE transmitted to other species; and PrP sequence polymorphism can influence which conformers form.
  • The same review notes that molecular strain typing is applied to vCJD diagnosis and cites the 1997 follow-up by Hill and colleagues for vCJD and BSE being one strain.
  • No PMC full text exists for the 1996 paper, and the Nature page requires login, so the quantitative results were not checked.

Timeline

  1. 1996Paper published in Nature 383:685-690 (issue dated 24 October 1996 in PubMed).
  2. 1997Follow-up by Hill et al., "The same prion strain causes vCJD and BSE", published in Nature 389:448-450.
  3. 2001Jackson and Collinge review cites the 1996 paper for vCJD glycoform ratios resembling BSE and for strain typing in diagnosis.

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Last checked 1 November 2026

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