Yuan-Qin Min

TL;DR: SFTSV NSs-mediated hijacking of STATs in IBs represents a novel mechanism of viral suppression of IFN signaling, highlighting the role of viral IBs as the virus-built “jail” sequestering some crucial host factors and interfering with the corresponding cellular processes.

TL;DR: In this article, the authors summarize and discuss the strategies of SARS-CoV-2 for evasion of innate immunity (particularly the antiviral IFN responses), understanding of which will facilitate not only the elucidation of infection and pathogenesis but also the development of antiviral intervention therapies.

TL;DR: It is shown that SFTSV infection induces an antiviral response accompanied by significant induction of antiviral and inflammatory cytokines and that RIG-I plays a main role in this induction by recognizing viral 5′-triphosphorylated RNAs and by signaling via the adaptor mitochondrial antiviral signaling protein.

TL;DR: It is reported that HRTV NSs (HNSs) also antagonizes IFN and cytokine induction and bolsters viral replication, and pulldown assays demonstrated that HNSs expression dose-dependently diminishes a TBK1-IRF3 interaction, further explaining the mechanism for H NSs function.

TL;DR: It is demonstrated that SFTSV infection results in substantial production of serum interferon-γ (IFN-γ) in patients and then that IFn-γ in turn exhibits a robust anti-SFTSV activity in cultured cells, indicating the potential role of IFN- γ in anti- SF TSV immune responses.