Recent experiments show that laboratory mice infected once with an inf
luenza A virus or with the murine parainfluenza type 1 virus, called t
he Sendai virus, have enhanced numbers of cytotoxic T-lymphocyte precu
rsors (>20x background) for life. Neither virus persists at the genome
level, and the mice are maintained under conditions where there is no
possibility of re-infection. These observations are highly relevant t
o any understanding of CD8(+) cell memory and suggest that the clonal
burst size associated with the primary challange is a key determining
factor.