Nucleic Acid Sensors Involved in the Recognition of HBV in the Liver–Specific in vivo Transfection Mouse Models—Pattern Recognition Receptors and Sensors for HBV

Cellular innate immune system recognizing pathogen infection is critical for the host defense against viruses. Hepatitis B virus (HBV) is a DNA virus with a unique life cycle whereby the DNA and RNA intermediates present at different phases. However, it is still unclear whether the viral DNA or RNA templates are recognized by the pattern-recognition receptors (PRRs) to trigger host antiviral immune response. Here in this article, we review the recent advances in the progress of the HBV studies, focusing on the nucleic acid sensors and the pathways involved in the recognition of HBV in the liver-specific in vivo transfection mouse models. Hydrodynamic injection transfecting the hepatocytes in the gene-disrupted mouse model with the HBV replicative genome DNA has revealed that IFNAR and IRF3/7 are indispensable in HBV eradication in the mice liver but not the RNA sensing pathways. Interestingly, accumulating evidence of the recent studies has demonstrated that HBV markedly interfered with IFN-β induction and antiviral immunity mediated by the Stimulator of interferon genes (STING), which has been identified as a central factor in foreign DNA recognition and antiviral innate immunity. This review will present the current understanding of innate immunity in HBV infection and of the challenges for clearing of the HBV infection.