Diverse mechanisms are used by viruses to inhibit, block, or evade the immune response (see review in reference 1). These include reduced expression of critical antigenic epitopes (eg, EBV in latency), genetic variation of class I–restricted CTL epitopes (HIV-1), clonal exhaustion of CTLs (HIV-1, lymphocytic choriomeningitis virus), downregulation of MHC class I and peptide–MHC complex expression (HSV, adenovirus, cytomegalovirus), production of an immunosuppressive cytokine (eg, IL-10–like factors by EBV), and downregulation of critical cytokines such as IL-12 (measles virus, HIV-1). Three studies, two published in this issue of The Journal of Experimental Medicine, describe a new mechanism whereby virus infection can subvert the immune response (2–4). Measles virus (MV) infection induces dendritic cell (DC) apoptosis and syncytia formation, leading to profound inhibition of IL-12 production by DCs and T cell proliferation. These studies may therefore provide some explanation for the dramatic immunosuppression that is often observed during MV infection. In addition, they highlight the dual and contrasting roles of DCs as potentiators of antiviral immune responses versus facilitators of disease pathogenesis and immunosuppression.