We found that the lack of response was not due to a general failure of the IECs to respond to infection, as both CaCo-2 and HT-29 expressed the PRRs shown to recognize CVBs (MDA5/RIG-I and TLR3; [9]) and responded to the cytosolic delivery of the viral dsRNA mimic poly (I:C) by inducing the expression of both type I and III IFNs. The gene discussed is RIGI; the disease is infection.