Mouse mammary tumor virus has developed strategies to exploit the immune response. It requires vigorous immune stimulation to achieve efficient infection. The infected antigen‐presenting cells present a viral superantigen on the cell surface which stimulates strong CD4‐mediated T‐cell help but CDS T‐cell responses are undetectable. Despite the high frequency of superantigen‐reactive T cells, the superantigen‐induced immune response is comparable to classical antigen responses in terms of T‐cell priming, T‐cell—B‐cell collaboration as well as follicular and extra‐follicular B‐cell differentiation. Induction of systemic anergy is observed, similar to classical antigen responses wbere antigen is administered systemically but does not influence the role of the superantigen‐reactive T cells in the maintenance of the chronic germinal center reaction. So far we have been unable to detect a cytotoxic T‐cell response to mouse mammary tumor virus peptide antigens or to the superantigen. This might yet represent another step in the viral infection strategy.