Figure 9.

Model for the interplays between SFTSV infection and IFN-γ-STAT1 signaling. SFTSV infection leads to the substantial production of IFN-γ which can direct anti-SFTSV action through induction of antiviral ISGs and other immune or inflammatory factors by IFN-γ-STAT1 signaling. In turn, the host anti-SFTSV response mounted by IFN-γ can be counteracted by the virus through the following two mechanisms: (1) NSs IB sequestration of STAT1 by the NSs-STAT1 interaction and (2) virus infection-induced downregulation of STAT1 protein abundance. Together, these viral and cellular actions reflect a complex arm race between SFTSV and its host, shedding lights on the virus-host interactions and viral pathogenesis.