Hepatitis A virus link to atopic disease

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. Risch, Gordon J. Freeman, Rosemarie H. DeKruyff and Dale T. Umetsu ()
Additional contact information
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

Nature, 2003, vol. 425, issue 6958, 576-576

Abstract: 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.

Date: 2003
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DOI: 10.1038/425576a

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