Rotavirus-induced immune responses, especially the T and B cell responses, have been extensively characterized; however, little is known about innate immune mechanisms required to control rotavirus infection. Rotavirus structural and nonstructural proteins have been detected in primary DCs from murine mesenteric lymph nodes and spleens [37, 38] , and murine bone marrowderived DCs have been shown to secrete type I IFN and tumor necrosis factor (TNF)a following rhesus (RRV) or bovine rotavirus (RF-81) challenge, respectively [39, 40] . Mature human monocytederived myeloid DCs (moDCs) have been demonstrated to be more susceptible to rotavirus infection than immature moDCs, although infection did not result in substantial cell death [41] . Additionally, infection did not induce moDC maturation, but instead promoted priming of Th1 cells [41] . A recent study of total human peripheral blood mononuclear cells (PBMCs) exposed to RRV or human rotavirus indicated that both myeloid DCs and pDCs are susceptible to infection, and that infection results in the secretion of IFNa, presumably from pDCs [42] . While increased levels of IFNa have also been correlated with a positive clinical outcome in infected children [43, 44] , several rotaviruses, including RRV, have recently been demonstrated to antagonize the production of type I IFN through the degradation of interferon regulatory factors (IRF)3, IRF5, and IRF7, and the inhibition of NFkB activation, by a viral nonstructural protein, NSP1 [45, 46, 47, 48] .