A team of US researchers has identified a vulnerability in the hepatitis B (HBB) virus that could open the door to new treatments. In a study published in the magazine ‘Cell‘, scientists from Memorial Sloan Kettering Cancer Center, Weill Cornell Medicine and the Rockefeller University (USA) have been able to block the virus’s ability to infect human liver cells in the laboratory using a compound already in clinical trials against cancer.
This finding feels the foundations for future studies in animal models and the development of new drugs.
Hepatitis B affects almost 5% of the world’s population and is one of the main causes of liver cancer. According to the World Health Organization, more than 250 million people suffer from chronic HBB infections, which causes more than one million deaths per year.
«One of the main challenges in the treatment of hepatitis B is that existing treatments can prevent the virus from making new copies of itself, but do not completely eliminate the virus of infected cells, which allows the virus to persist in the Liver and maintain chronic infection, ”says hepatologist and virologist Robert Schwartz, from Weill Cornell Medicine, whose laboratory contributed his experience biological and clinical in the virus, as well as in the human liver cell models used in the study.
The hepatitis B vaccine is also effective, but to maintain immunity, reinforcement doses are usually necessary. In addition, it does not help people who are already infected. This happens, for example, due to the transmission of mother to child virus, something very common in developing countries. Access to vaccines and treatment is also more limited in some parts of Africa and Asia, where infection rates are higher.
The team has investigated a mystery of decades: how the hepatitis B virus manages to establish a productive infection in liver cells. They discovered that for a key protein called X -Sencial protein for virus replication – HBB DNA should be organized in human histone and histone complexes. This mechanism is essential for virus survival and, when interrupting it, a new therapeutic approach could be developed.
The study tested five small molecules capable of altering chromatin formation. Only one of them, CBL137, blocked the production of the X protein in liver cells.
This drug, which is already in clinical trials against cancer, proved to be effective in doses much lower than those used in cancer studies, only affecting the virus without damaging human cells.
The researchers point out that, if these results are confirmed with additional studies, CBL137 could represent a potential cure for chronic HBB infection. In addition, this approach could be applied to other chromatinized DNA viruses, such as herpes viruses and human papilloma.
The next step will be to evaluate the safety and efficacy of CBL137 in animal models, although the options are limited due to the narrow range of species that HBV can infect.
The study highlights the importance of interdisciplinary collaboration among the institutions involved. “This project would not have been possible without the combination of experience in viral, epigenetic and genomic biology,” the researchers write.
With this advance, researchers hope to get closer and more to a definitive solution for hepatitis B, a disease that affects millions of people worldwide.
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