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)‐α/β, cytotoxicity and IFN‐γ production by natural killer cells, interleukin‐12 induction, and depletion of non‐specific T cells early during virus infection need further evaluation.