The potential immune regulation benefit of CpAMs beyond HBV suppression

Current approved antiviral therapies for chronic hepatitis B virus (HBV) infection are limited to either nucleotide or nucleoside analogues or pegylated interferon α, all of which can efficiently suppress HBV replication and reduce the risk of chronic HBV-related liver diseases.1 However, these therapies do not affect the transcriptional activity of intrahepatic covalently closed circular DNA (cccDNA), which causes viral persistence, and thus fail to eradicate the virus. Novel approaches targeting alternative steps in the HBV life cycle and specific virus–host cell interactions are being investigated, with the goal of achieving a functional cure.