Hill AF et al. 1997, The same prion strain causes vCJD and BSE (Nature 389:448-450, PMID 9333232, doi 10.1038/38925)

A 1997 Nature letter from the Collinge group in London that compared the transmission and molecular behaviour of variant CJD with BSE and concluded that the two are consistent with one prion strain, so that vCJD is the human counterpart of BSE. It appeared in the same period as an independent mouse study from Edinburgh with the same conclusion. The atlas holds it as a landmark strain-typing paper. Only the abstract could be read, so the experimental detail below is limited to what later papers say about it.

Key facts

  • The citation is confirmed: eight authors (Hill, Desbruslais, Joiner, Sidle, Gowland, Collinge, Doey, Lantos), Nature volume 389 issue 6650, pages 448-450 (the record adds 526), published 2 October 1997, PMID 9333232, doi 10.1038/38925.
  • The abstract states that epidemiology, clinical and pathological studies and analysis of PrPSc supported a causal link between vCJD and BSE, yet the question was still debated.
  • Its stated conclusion is that the biological and molecular transmission properties of vCJD are consistent with vCJD being the human counterpart of BSE; the wording is "consistent with", not a claim of proof.
  • The abstract frames strain identity as shown by behaviour in laboratory animals and by physical and chemical features of PrPSc, which is the basis for comparing vCJD with BSE.
  • PubMed lists the item as a Comment-type article without an abstract and with no erratum; Europe PMC lists it as Letter and Comment.
  • A separate Nature paper by Bruce, Will, Ironside and colleagues (pages 498-501) reported interim mouse transmissions and also called it strong evidence that one agent strain underlies BSE and vCJD.
  • The 2002 EMBO Journal paper from the same group says the 1997 work found that vCJD in mice expressing human PrP with valine at codon 129 gave a new PrPSc pattern, attributed to a strain switch from a codon 129 mismatch.
  • That 2002 paper also showed that BSE in methionine-129 human PrP mice can give either the vCJD pattern or a sporadic-CJD-like type 2 phenotype.
  • A 2012 study of vCJD isolates from five countries found an identical blot profile and supports a single agent strain for vCJD, citing Hill 1997 as background.

Timeline

  1. 1997Bruce et al. companion paper on mouse transmissions of vCJD and BSE appeared in the same journal volume (month not confirmed).
  2. 1997Hill et al. published in Nature 389:448-450.
  3. 2002Asante et al. reported that BSE can propagate as a vCJD-like or sporadic-CJD-like strain in human PrP transgenic mice, building on the 1997 work.
  4. 2012Diack et al. reported constant vCJD transmission properties across five countries.

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Last checked 1 November 2026

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