Technology Summary

The present invention addresses the role of the capsid protein in the cccDNA formation of the Hepatitis B virus. Certain HBc (Hepatitis B core protein) mutations were found to alter the integrity of mature nuclear capsid (NC). Those mutations enhanced cccDNA formation and increased the nuclear cccDNA pool. The increased levels of cccDNA formed by these HBc mutants will facilitate efforts to target this critical viral episome for antiviral development. These findings provide the rationale to manipulate the integrity of mature NCs as novel ways to eliminate viral persistence by diminishing levels of viral nuclear episomes. The invention opens the opportunity to designing new antiviral strategies to cure persistent HBV infection.