For example, autopsies of children with fatal RSV infections show a relative deficiency of CD8 T cell responses[1]; recipients of allogeneic bone marrow and lung transplants have difficulty in controlling RSV replication and often have fatal outcomes as a consequence of syncytium-forming pneumonia[2, 3]; and in patients with severe combined immunodeficiency (SCID), RSV infection results in persistent virus shedding that can be controlled with T cell reconstitution[4, 5]. Here, CD8A is linked to severe combined immunodeficiency.