The concept of heterologous T cell immunity postulates that nonspecific memory T cells recruited and reactivated in the context of an unrelated virus infection may contribute to protective antiviral immunity. Pulmonary infection with respiratory syncytial virus (RSV) of mice immune to lymphocytic choriomeningitis virus (LCMV) leads to substantial recruitment of systemic LCMV-specific memory CD8 T cells to the lung. Using a sensitive TCR-transgenic model, we show that such "bystander" recruitment to the RSV-infected lung could induce a single round of cell division among LCMV-specific T cells. However, it did not change their activation status as assessed by expression of surface markers, the extent or kinetics of IFN-gamma production and cytolytic effector function. Moreover,recruitment of LCMV-specific bystander T cells not only failed to enhance immunity to RSV, but significantly delayed virus elimination and slightly enhanced RSV-induced weight loss in non-transgenic BALB/c mice. This correlated with a delay in the recruitment of RSV-specific T cells to the lung. These data show that bystander recruitment of heterologous T cells is not necessarily accompanied by bystander activation. More importantly, bystander recruitment of systemic memory T cells can impair antiviral immunity, presumably by interference with the recruitment of specific T cells.