Hepatitis B Virus Polymerase Blocks Pattern Recognition Receptor Signaling via Interaction with DDX3: Implications for Immune Evasion

摘要: Viral infection leads to induction of pattern-recognition receptor signaling, which interferon regulatory factor (IRF) activation and ultimately (IFN) production. To establish infection, many viruses have strategies evade the innate immunity. For hepatitis B virus (HBV), causes chronic in liver, evasion strategy remains uncertain. We now show that HBV polymerase (Pol) blocks IRF indicating Pol is viral molecule effectively counteracts host immune response. In particular, inhibits TANK-binding kinase 1 (TBK1)/IκB kinase-e (IKKe), effector kinases signaling. Intriguingly, TBK1/IKKe activity by disrupting interaction between IKKe DDX3 DEAD box RNA helicase, was recently shown augment activity. This unexpected role may explain how evades response early phase infection. A therapeutic implication this work a interfere with Pol-DDX3 might lead resolution life-long persistent