Consistent with the general resistance to rotavirus infection, pDCs retained several important functional abilities following RRV exposure, as evidenced by their activation, maturation and cytokine production. Evidence of this functionality was observed primarily in the major NSP2bystander population, although activation and maturation were significantly enhanced in the few NSP2 + pDCs, as well. The induction of this phenotype by inactivated RRV further indicates that the pDCs are responding to the presence of input virus or to secreted factors, and not to viral replication. The upregulation of DC costimulatory and maturation markers suggests antigen presentation to T cells is preserved, in line with previous reports that pDCs are necessary for stimulation of IFNc-secreting memory T cells [42] . The antigen presentation hypothesis is supported by increased expression of CD86 and CD83 on NSP2 + pDCs compared to bystander pDCs, indicating that the presence of virus enhances this phenotype. Conversely, IFNa/b production is impaired in NSP2 + pDCs. Combined with decreased IRF7 phosphorylation in NSP2 bright pDCs, this suggests the direct inhibition of the type I IFN response by rotavirus replication, as has been previously observed in fibroblasts and epithelial cells [45, 46, 47, 48] .