Duck IFNγ Restricts Duck Tembusu Virus Replication by Disrupting Viral RNA Synthesis/Translation

, is a major avian pathogen that imposes enormous economic losses on the global duck industry, necessitating urgent development of effective countermeasures. Although Interferon-gamma (IFNγ) is a crucial broad-spectrum antiviral cytokine, its role against DTMUV infection remains mechanistically undefined. In this study, we first demonstrated that DTMUV induced duck IFNγ (duIFNγ) production in immune and non-immune cells. Importantly, duIFNγ exhibited a dual anti-DTMUV function in vitro: it not only prevented viral replication but also displayed the capacity to clear existing virus from infected cells. Mechanistically, cycloheximide (CHX) experiments confirmed that duIFNγ exerts its antiviral effect by disrupting the viral RNA synthesis/translation phase. Furthermore, transcriptomic profiling (RNA-seq) precisely revealed that duIFNγ restricts DTMUV replication by activating multiple host defense pathways, notably Programmed Cell Death (e.g., Caspase signaling) and the RIG-I-like Receptor (RLR) signaling pathways. Collectively, these findings provide critical insights into the function and mechanism of duIFNγ in combating DTMUV in vitro, laying a robust theoretical foundation for exploring duIFNγ or its induced effectors as novel therapeutics for DTMUV infection.