• 1 January 1981
    • journal article
    • research article
    • Vol. 33 (3), 381-395
Abstract
A 2-locus disease model is presented in which a marker locus interacts epistatically with another unlinked trait to cause the disease. Such a model can lead to disease-marker associations and distortions in the sharing of marker types among affected family members. These effects are quantified. In HLA-disease associations, this model is presented as an alternative to the hitchhiking theory of tight linkage leading to linkage disequilibrium.