pDCs play a vital role in the generation of innate and adaptive immunity following viral infection, primarily through the production of large quantities of IFNa in response to stimulus of TLR7 or TLR9 PRRs by ssRNA or DNA PAMPs, respectively. Traditional receptors for dsRNA, such as RIG-I, MDA5 and TLR3, are largely thought to not play a role in the initiation of the IFN response in human pDCs [2, 3, 4, 5, 6, 7, 8, 9] . Although Newcastle disease virus normally elicits an IFNa response in murine pDCs through triggering TLR7, RIG-I-like helicases have been recently implicated in IFNa induction by replicating virus in murine pDCs lacking the IFN receptor [14] . Hence, the mechanisms governing efficient IFNa induction in these cells by transcriptionally inactivated, replication-incompetent dsRNA rotavirus are not yet understood. As rotaviruses represent a large burden of human disease, it will be important to better understand the immune mechanisms underlying their recognition and subsequent generation of antiviral immunity.