Inhibition of HBV Transcription From cccDNA With Nitazoxanide by Targeting the HBx–DDB1 Interaction

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Hepatitis B virus (HBV) infection leads to chronic hepatitis B (CHB) in approximately 250 million people worldwide, putting them at high risk for developing cirrhosis and hepatocellular carcinoma. HBV is a partially double-stranded DNA virus that belongs to the Hepadnaviridae family. After entry into host cells, the viral genome is transported into the nucleus and converted to a covalently closed circular DNA (cccDNA), which serves as the template for all HBV viral RNAs. Currently available HBV antiviral drugs inhibit the reverse transcription of HBV pregenomic RNA but fail to suppress the established cccDNA reservoir in infected hepatocytes, resulting in viral rebound after therapy. In addition, HBV surface antigen hepatitis B surface antigen expressed from the cccDNA maintains immune tolerance to prevent induction of antibodies to hepatitis B surface antigen, which are critical for a functional cure of CHB in patients.

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