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Hepatitis A virus link to atopic disease

Author

Listed:
  • Jennifer J. McIntire

    (Stanford University)

  • Sarah E. Umetsu

    (Stanford University)

  • Claudia Macaubas

    (Stanford University)

  • Elizabeth G. Hoyte

    (Stanford University)

  • Cengiz Cinnioglu

    (Stanford University)

  • Luigi L. Cavalli-Sforza

    (Stanford University)

  • Gregory S. Barsh

    (Stanford University)

  • Joachim F. Hallmayer

    (Stanford University)

  • Peter A. Underhill

    (Stanford University)

  • Neil J. Risch

    (Stanford University)

  • Gordon J. Freeman

    (Dana-Farber Cancer Institute, Harvard University)

  • Rosemarie H. DeKruyff

    (Stanford University)

  • Dale T. Umetsu

    (Stanford University)

Abstract

Atopic diseases, including asthma, allergic rhinitis and atopic dermatitis, are caused by both environmental and genetic factors. Here we show that infection by hepatitis A virus (HAV) may protect individuals from atopy if they carry a particular variant of the gene that encodes TIM-1 (also known as HAVcr-1) — the cell-surface receptor used by HAV to infect human cells1. Exposure to HAV is associated with poor hygiene, large family size and attendance at day-care centres, all factors that are also inversely associated with atopy2,3,4,5,6. Our discovery indicates that interaction between HAV and TIM-1 genotype may contribute to the aetiology of atopic diseases, and provides a mechanism to account for the hygiene hypothesis.

Suggested Citation

  • Jennifer J. McIntire & Sarah E. Umetsu & Claudia Macaubas & Elizabeth G. Hoyte & Cengiz Cinnioglu & Luigi L. Cavalli-Sforza & Gregory S. Barsh & Joachim F. Hallmayer & Peter A. Underhill & Neil J. Ris, 2003. "Hepatitis A virus link to atopic disease," Nature, Nature, vol. 425(6958), pages 576-576, October.
    • Handle: RePEc:nat:nature:v:425:y:2003:i:6958:d:10.1038_425576a
    DOI: 10.1038/425576a
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