FIG 7.

Schematic summary. Monocytes/macrophages are the key targets of TMUV in its arthropod-borne transmission route, which is essential for viral replication, transmission, and pathogenesis. Upon TMUV infection, monocytes/macrophages are successfully alerted through the activation of major PRR signaling pathways, which results in dramatic upregulation of IFN-β transcription. To survive in monocytes/macrophages, TMUV attenuates type I IFN-mediated antiviral immune responses by preventing the elevation of IFN-α transcription and reducing the translation and protein stability of IFN-β. Meanwhile, TMUV inhibits the transcription of NADPH oxidase subunits and enhances the transcription of antioxidant genes by promoting the nuclear translocation of Nrf2 to maintain a stable redox state in monocytes/macrophages.