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HLA-DQ7 antigen and resistance to variant CJD

Author

Listed:
  • Graham S. Jackson

    (MRC Prion Unit, Institute of Neurology, University College London)

  • Jonathan A. Beck

    (MRC Prion Unit, Institute of Neurology, University College London)

  • Cristina Navarrete

    (National Blood Service, Histocompatibility and Immunogenetics
    Royal Free and University College Medical School)

  • Juliette Brown

    (National Blood Service, Histocompatibility and Immunogenetics)

  • P. Margaret Sutton

    (Oxford Transplant Centre, Oxford Radcliffe Hospitals)

  • Marcela Contreras

    (National Blood Service, Histocompatibility and Immunogenetics
    Royal Free and University College Medical School)

  • John Collinge

    (MRC Prion Unit, Institute of Neurology, University College London)

Abstract

Variant Creutzfeldt–Jakob disease (vCJD) in humans is caused by a bovine spongiform encephalopathy (BSE)-like prion strain, and so far about 100 of the many people exposed to BSE prions have developed the condition. Here we show that there is a significantly reduced frequency of the human leukocyte antigen (HLA) class-II type DQ7 in patients with vCJD, but not in those with classical CJD. This apparently protective genetic factor should aid differential diagnosis and may have important implications for understanding host susceptibility to infection by BSE prions, and the distinctive pathogenesis of vCJD, as well as in the identification of targets for prevention and therapy of vCJD.

Suggested Citation

  • Graham S. Jackson & Jonathan A. Beck & Cristina Navarrete & Juliette Brown & P. Margaret Sutton & Marcela Contreras & John Collinge, 2001. "HLA-DQ7 antigen and resistance to variant CJD," Nature, Nature, vol. 414(6861), pages 269-270, November.
    • Handle: RePEc:nat:nature:v:414:y:2001:i:6861:d:10.1038_35104694
    DOI: 10.1038/35104694
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