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Review
. 2023 Aug 1;13(8):1208.
doi: 10.3390/biom13081208.

Chronic Hepatitis B Infection: New Approaches towards Cure

Mojisola Ogunnaike  1   2 , Srijanee Das  1   2 , Samiksha S Raut  1 , Ashrafi Sultana  1 , Mohammad Ullah Nayan  1 , Murali Ganesan  1   3 , Benson J Edagwa  1 , Natalia A Osna  1   3 , Larisa Y Poluektova  1
Affiliations
Review

Chronic Hepatitis B Infection: New Approaches towards Cure

Mojisola Ogunnaike et al. Biomolecules. .

Abstract

Chronic hepatitis B virus (HBV) infection leads to the development of cirrhosis and hepatocellular carcinoma. Lifelong treatment with nucleotides/nucleoside antiviral agents is effective at suppressing HBV replication, however, adherence to daily therapy can be challenging. This review discusses recent advances in the development of long-acting formulations for HBV treatment and prevention, which could potentially improve adherence. Promising new compounds that target distinct steps of the virus life cycle are summarized. In addition to treatments that suppress viral replication, curative strategies are focused on the elimination of covalently closed circular DNA and the inactivation of the integrated viral DNA from infected hepatocytes. We highlight promising long-acting antivirals and genome editing strategies for the elimination or deactivation of persistent viral DNA products in development.

Keywords: antivirals; chronic hepatitis B; gene editing; hepatitis B virus.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the collection, analyses, or interpretation of published literature, in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Therapeutic interventions for the prevention of end-stage liver diseases by effective suppression of HBV replication (1) and elimination of viral DNA products (2).
Figure 2
Figure 2
Current therapeutic strategies for HBV treatment and cure. Entry inhibitors block the NTCP receptors preventing viral entry into hepatocytes; Base editing tools selectively rewrite persistent HBV cccDNA and integrants into dysfunctional phenotype; RNA interference targets HBV RNA to prevent its translation into viral proteins; Capsid assembly modulators block the encapsidation Pol-pgRNA and cccDNA replenishment; and Ultralong-acting Nucleotide Reverse Transcriptase Inhibitors (ULA-NTRI) directly inhibit reverse transcription of HBV RNA, thereby providing sustained suppression of HBV DNA synthesis and chromosomal DNA integration. Figure created with BioRender.
See this image and copyright information in PMC

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