Given that CD8 T cells are crucial in the control of CVB3-myocarditis [29], [32], absolute CD8 T cell numbers for CVB3 epitopes are low and detection of specific CD8 T cell frequencies is limited in this infection model, adoptive transfer studies of CVB3-memory CD8 T cells from IP-deficient and IP-competent mice appeared to be the most reliable approach to address the effect of IP-deficiency on CD8 T cell function. This evidence concerns the gene CD8A and myocarditis.