Aging is associated with an increased morbidity to virus infections as well as a delay in clearance of symptoms after infection. Studies of sublethal virus infections of aged mice closely mirror the human situation: there is a delay in clearance of virus. The delay in virus clearance is accompanied by a delay and a decrease in T-cell response, particularly of CD8(+) T cells. Intrinsic alterations of T cells of aged mice contribute to this decrease in virus-specific T-cell response; however, evidence suggests that environmental or innate components of the aged host also influence this age-associated decline in clearance of virus. While the changes in the adaptive immune response have been carefully described, the early events in the generation of the T-cell response after virus infection have received limited attention. Importantly, age-associated changes in the innate response to virus infection, particularly production of and response to interferon (IFN)-alpha/beta, cytotoxicity and IFN-gamma production by natural killer cells, interleukin-12 induction, and depletion of non-specific T cells early during virus infection need further evaluation.