Antiviral Drugs Against Severe Fever With Thrombocytopenia Syndrome Virus Infection

Takayama-Ito, Mutsuyo; Saijo, Masayuki

IFN-γ is the only member of type II IFNs. It stimulates macrophage and dendritic cells to induce direct antimicrobial activities by regulating antigen processing and presentation pathways. It was initially thought that activated T cells and activated natural killer cells were the only relevant source of IFN-γ; however, macrophages and dendritic cells can also be stimulated to produce IFN-γ in vitro under certain conditions (Thäle and Kiderlen, 2005) . Because IFN-γ can directly stimulate the expression of some potential antiviral IFN-stimulating proteins by the STAT1 signaling, it plays an important role in viral infection. Ning et al. (2019) used enzyme-linked immunosorbent assays to demonstrate that SFTSV infection caused a substantial production of serum IFN-γ in patients with SFTS. In turn, IFN-γ exhibited a robust anti-SFTSV activity in cultured cells. Thereafter, they evaluated the efficacy of IFN-γ as an anti-SFTSV drug in vivo in a suckling mouse model, which showed that IFN-γ treatment prior to SFTSV infection significantly reduced mortality, protecting ∼25% of animals from death, whereas all the untreated mice died within 13 days of the SFTSV challenge. When IFN-γ was administrated post SFTSV infection, 100% of the mice died from the virus.