In summary, the current study demonstrates that the type II IFN, IFN-γ, which can be substantially induced during SFTSV infection has anti-SFTSV efficacy both in vitro and in vivo; in turn, the antiviral activity is counteracted by SFTSV through NSs-STAT1 interaction-mediated sequestration of STAT1 in viral IBs and virus infection-induced downregulation of STAT1 protein abundance. The gene discussed is IFNG; the disease is viral infectious disease.