Research Opens the Door to a Possible Treatment for Hepatitis B

Research aimed at understanding how the hepatitis B virus infects liver cells has identified a vulnerability that could open the way to new treatments for the disease. The study, published in the journal Cell, was led by Memorial Sloan Kettering Cancer Center (MSK), Weil Cornell Medicine and Rockefeller University (United States).

The findings reveal that the team was able to disrupt the ability of the hepatitis B virus to infect human liver cells using a compound that is already in clinical trials for cancer treatment. This lays the groundwork for future studies with animal models and the possible development of drugs to treat the disease.

The focus of the research was a key viral gene that encodes a protein called X. This gene is essential for hepatitis B to establish a productive infection in host cells and activate the expression of its viral genes. Protein X is also considered the virus’s oncogene, as it plays a pivotal role in the disease’s progression to cancer.

That is because protein X degrades host proteins involved in DNA repair, which not only prevents the immune system from silencing their activity, but increases the chances that cells will accumulate DNA errors over time, thus promoting the development of cancer.

Hepatitis B affects 5% of the world’s population

Chronic hepatitis B virus (HBV) infection is incurable and responsible for liver disease and hepatocellular carcinoma. HBV affects nearly 5% of the world’s population, with more than 250 million people suffering from chronic hepatitis B infections.

According to the World Health Organization (WHO), the virus causes more than one million deaths a year, making it the second deadliest infection globally. Although the hepatitis B vaccine is effective, it requires booster doses and offers no protection to people already infected. In addition, access to vaccines and treatments is limited in countries in Africa and Asia , where infection rates are especially high.

According to the study, in order for the X protein to be produced, the virus’ DNA must be organized into nucleosomes, the building blocks of chromatin, which form chromosomes. The researchers discovered that the presence of nucleosomes in the viral genome is essential for the transcription of the RNA that gives rise to the X protein. This discovery has allowed them to better understand how the X gene is regulated and how hepatitis B infection is established.

If the formation of these chromatin structures can be altered, it could modify the virus’s ability to initiate and maintain infection. The team tested five small molecule compounds known to alter chromatin formation. Only one of these blocked the production of the X protein in liver cells: CBL137, a drug used in the treatment of cancer.

This compound worked at very low concentrations, affecting only the virus and not human cells. The next step will be to conduct clinical trials in animals to evaluate the efficacy of CBL137, although unfortunately few species are susceptible to hepatitis B infection.

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(Featured image by National Cancer Institute via Unsplash)

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First published in Gaceta Medica. A third-party contributor translated and adapted the article from the original. In case of discrepancy, the original will prevail.

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