Mouse mammary tumor virus has developed strategies to exploit the immune re
sponse. It requires vigorous immune stimulation to achieve efficient infect
ion. The infected antigen-presenting cells present a viral superantigen on
the cell surface which stimulates strong CD4-mediated T-cell help but CD8 T
-cell responses are undetectable. Despite the high frequency of superantige
n-reactive T cells, the superantigen-induced immune response is comparable
to classical antigen responses in terms of T-cell priming, T-cell-B-cell co
llaboration as well as follicular and extra-follicular B-cell differentiati
on Induction of systemic anergy is observed, similar to classical antigen r
esponses where antigen is administered systemically but does not influence
the role of the superantigen-reactive T cells in the maintenance of the chr
onic germinal center reaction. So far we have been unable to detect a cytot
oxic T-cell response to mouse mammary tumor virus peptide antigens or to th
e superantigen. This might yet represent another step in the viral infectio
n strategy.