Although the exact mechanisms of murine leukemia virus (MuLV)-induced
lymphomagenesis have yet to be elucidated, it is clear that the immune
reponse to viral proteins plays a critical role in this disease proce
ss. The parameters for lymphomagenesis are governed by an inverse rela
tionship between viral persistence and immune responsiveness. MuLV hav
e evolved ways to avoid immune detection either by altering their own
genome or by altering the host environment. In addition, the intrathym
ic replication of MuLV during thymocyte maturation and immune selectio
n plays an important role in T cell repertoire development and immune
inhibition. These viruses have served as a highly effective experiment
al model in understanding the many pathways by which MuLV have overcom
e immune detection and thereby led to lymphomagenesis.