Decades-Old Hepatitis B Mystery Unveils Promising New Treatment: Study
In their effort to answer a decades-old biological question about how the hepatitis B virus (HBV) is able to establish infection of liver cells, research led by Memorial Sloan Kettering Cancer Center (MSK), Weill Cornell Medicine, and The Rockefeller University identified a vulnerability that opens the door to new treatments.
The team successfully disrupted the virus’s ability to infect human liver cells in the laboratory using a compound already in clinical trials against cancer — laying the groundwork for animal model studies and potential drug development based on their insights, according to findings published in Cell journal.
Chronic hepatitis B virus (HBV) infection is an incurable pathogen responsible for causing liver disease and hepatocellular carcinoma. During the genesis of infection, HBV establishes an independent minichromosome consisting of the viral covalently closed circular DNA (cccDNA) genome and host histones. The viral X gene must be expressed immediately upon infection to induce degradation of the host silencing factor, the Smc5/6 complex.
However, the relationship between cccDNA chromatinization and X gene transcription remains poorly understood. By establishing a reconstituted viral minichromosome platform, the researchers found that nucleosome occupancy in cccDNA regulates X transcription.
They corroborated these findings in situ and further showed that the chromatin-destabilizing molecule CBL137 inhibits full-length X transcription and HBV infection in primary human hepatocytes. The results of the study shed light on a long-standing paradox and represent a potential therapeutic approach for the treatment of chronic HBV infection.
The research was led by chemical biologist Yael David, PhD, at MSK, working together with hepatologist and virologist Robert Schwartz, MD, PhD, at Weill Cornell Medicine and Viviana Risca, PhD, at The Rockefeller University.
Ref: Nicholas A. Prescott,Tracy Biaco,Andrés Mansisido et al. A nucleosome switch primes hepatitis B virus infection, Cell: DOI: 10.1016/j.cell.2025.01.033
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