IL1β signaling mediates the interaction between hepatitis B and C viruses

Our findings reveal a macrophage-derived, IFN-independent mechanism by which HCV suppresses HBV infection, mediated through IL1β. These insights highlight the complex crosstalk between hepatotropic viruses during coinfection and suggest that targeting IL1β-regulated pathways may offer therapeutic potential to prevent HBV reactivation in DAA-treated patients.