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Rotavirus (RV) replication in intestinal epithelial cells (IECs) in vivo is robust despite the vigorous activation of local early host interferon (IFN) responses. Using single cell microfluidics qRT-PCR coupled with flow sorting, we recently demonstrated that homologous RV efficiently inhibits IFN induction in single infected and bystander villous IECs in vivo and, using genetic approaches, associated this function with the RV NSP1 protein. Paradoxically, RV also induces robust type I IFNs in the intestinal hemaotopoietic compartment in a relatively replication-independent manner raising the possibility that RV replication and spread in IECs occurs despite exogenous stimulation of the STAT1-mediated IFN signaling pathway. However, viral factor(s) responsible for the possible inhibition of STAT1 function are unknown. Here we report the ability of RV to mediate direct and remote inhibition of IFN-mediated STAT1 activation …