Reactivation of cytomegalovirus ( CMV) can induce T cells to undergo immune senescence, a mechanism of aging. After CMV infection of immunocompetent hosts, it persists in bone marrow. CMV is stimulated and propagates into circulation via differentiation?dependent reactivation throughout life. This article compares and reviews the immune status of human and nonhuman primates after CMV infection, the immune escape mechanisms, and the relationship with immune senescence. Such information may provide a basis for establishing models of immune senescence and the development of drugs and vaccines.