This model revealed a number of important findings: (i) prior viral infection resulted in massively increased recruitment of CD44hi CD8+ T cells into allogeneic, but not syngeneic, heart grafts; (ii) such enhanced recruitment was associated with substantially increased timing and severity of histologically-defined rejection; (iii) a substantial number of viral-specific memory CD8+ T cells cross-reacted to allogeneic, but not syngeneic, heart grafts; (iv) the cross-reactivity of viral-specific CD8+ T cells with alloantigen varied depending upon the viral epitope. The gene discussed is CD8A; the disease is viral infectious disease.