Abstract
Why is there an urgent need to develop therapeutic alternatives for chronic hepatitis B? Despite the existence of an effective vaccine, chronic HBV infection is still a global public health problem, with at least 370 million virus carriers who are at high risk of developing cirrhosis and hepatocellular carcinoma. The efficacy of current anti-HBV therapies, which rely on IFN-α and nucleoside analogs (lamivudine and adefovir), is limited by the emergence of drugresistant mutants and the persistence of intranuclear covalently closed circular viral DNA (cccDNA) forms, which are responsible for viral relapse after treatment withdrawal [1]. Therefore, this cccDNA pool, which can be considered as a viral minichromosome, plays a crucial role in the persistence of HBV infection, and its elimination remains a major clinical challenge. In this regard, an increasing body of evidence from different animal models, such as HBV-replicating transgenic mice, HBV-infected chimpanzee, woodchuck HBV (WHV)-infected woodchucks and duck HBV (DHBV)-infected ducks, indicate that at least partial viral RNA and cccDNA clearance can be achieved by two mechanisms that are not mutually exclusive:
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