This grouping enabled us to test the hypothesis that this association of specific viruses with breast cancer immunogenetics may be due to lower virus binding affinity to HLA molecules, thus delaying the elimination of virus directly (via HLA-I—CD8 + engagement leading to death of the infected cell) and/or indirectly (via HLA-II—CD4 + engagement leading to antibody production). The gene discussed is CD4; the disease is breast carcinoma.