SUPERANTIGEN-INDUCED IMMUNE STIMULATION AMPLIFIES MOUSE MAMMARY-TUMORVIRUS-INFECTION AND ALLOWS VIRUS TRANSMISSION

Endogenous and infectious mouse mammary tumor viruses (MMTVs) encode i n their 3' long terminal repeat a protein that exerts superantigen act ivity; that is, it is able to interact with T cells via the variable d omain of the T cell receptor (TCR) beta chain. We show here that trans mission of an infectious MMTV is prevented when superantigen-reactive cells are absent through either clonal deletion due to the expression of an endogenous MTV with identical superantigen specificity or exclus ion due to expression of a transgenic TCR beta chain that does not int eract with the viral superantigen. A strict requirement for superantig en-reactive T cells is also seen for a local immune response following MMTV infection. This immune response locally amplifies the number of MMTV-infected B cells, most likely owing to their clonal expansion. Co llectively, our data indicate that a superantigen-induced immune respo nse is critical for the MMTV life cycle.