During infection, sfRNAs accumulate to high levels in the cell and contribute to flavivirus infection through multiple mechanisms (20, 22); specific sfRNA structures stall not only XRN1 but also other 5′−3′ exonucleases and alter mRNA stability dynamics (23, –, 25), sfRNA binds to a variety of host proteins that play roles in viral replication and translation (26, –, 29), and there is growing evidence that the sfRNAs are involved in blocking host innate immune response (30, –, 32). The gene discussed is XRN1; the disease is infection.