The rules for T‐cell‐mediated control of viruses that infect via the respiratory mucosae show both common themes and differences depending on the nature of the pathogen. Virus‐specific CD8⁺ cytotoxic T lymphocytes (CTLs) are the key effectors of virus clearance in mice infected with both negative strand RNA viruses (influenza and Sendai) and a DNA virus, the murine γ‐herpesvirus68 (MHV‐68). Recently completed experiments establish that these activated CD8⁺ T cells indeed operate primarily via contact‐dependent lysis, Perform‐mediated cytotoxicity seems to be the preferred mode, though a Fas‐based mechanism can apparently serve as an alternative mechanism. Immune CD4⁺ T cells functioning in the absence of the CD8⁺ subset cannot eliminate MHV‐68 from lung epithelial cells, are somewhat less efficient than the CD8⁺ CTLs at clearing the RNA viruses, and are generally ineffectual in mice that lack B lymphocytes. Though cytokine secretion by CD4⁺ and CD8⁺ T cells in the virus‐infected king may promote both T‐cell extravasation and macrophage activation, such processes are not alone sufficient to deal consistently with any d these infections. However, CD4⁺ T help is mandatory for an effective B‐cell response, and can operate lo promote the clonal expansion of virus‐specific CD8⁺ T cells in the lymph nodes and spleen. Furthermore, a concurrent CD4⁺ T‐cell response seems to be essential for maintaining continued CD8⁺ T‐cell surveillance and effector capacity through the persistent, latent phase of MHV‐68 infection in B cells. Thus, the evidence to date supports a very traditional view: CD8⁺ T cells function mainly as killers and the CD4⁺ T cells as helpers in these respiratory virus infections.