pDCs possess a seemingly unique phenotype in the context of rotavirus infection, as the ability of NSP1 to degrade multiple IRFs appears to subvert the type I IFN response in many other cells, including epithelial and fibroblastic cells [45, 46, 62] . Presumably, the constitutive expression of IRF7 in pDCs [63] allows for rapid induction of IFNa following rotavirus exposure, thus effectively suppressing viral replication-and the production of NSPs-in the majority of pDCs through the establishment of a largely paracrineinduced antiviral state. This conclusion is supported by the observed lack of significant increase in the NSP2 + or IFNa + pDC populations when the moi is increased to 25 or 100 (data not shown). Importantly, the decrease in IFNa and pIRF7 in pDCs expressing high levels of NSP2 illustrates that the local suppression of the interferon response by actively replicating virus [45, 46, 47, 48] is conserved in human pDCs at an individual cell level. However, inhibition in this minor population is unlikely to substantially modulate the amount of cytokine produced by the total pDC population. The present study provides the first formal demonstration of type I IFN inhibition in primary human cells in which rotavirus replicates.