Abstract
To effectively combat hepatitis B virus (HBV), it is imperative to develop potent antiviral medications targeting covalently closed circular DNA (cccDNA). Our investigation aimed to assess the impact of SARS-CoV-2 nsp13 on HBV replication across diverse HBV models, confirming its ability to significantly reduce several HBV replication markers. Additionally, our identification of the interaction between nsp13 and SMC4 opens the door for further mechanistic exploration. This marks a paradigm shift in our approach to HBV antiviral therapy, introducing an entirely novel perspective. Our findings propose a novel strategy for developing anti-HBV drugs that specifically target HBV cccDNA.
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