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 Feb. 20 in Cell.
Hepatitis B is a liver infection that affects almost 5% of the world’s population. It causes long-term damage to liver cells and is one of the leading causes of liver cancer. More than 250 million people worldwide have chronic HBV infections and the virus causes more than 1 million deaths a year, making it the second most deadly infection worldwide, according to the World Health Organization.
The research was led by chemical biologist Dr. Yael David at MSK, hepatologist and virologist Dr. Robert Schwartz at Weill Cornell Medicine and Dr. Viviana Risca at The Rockefeller University.
This project started from our fundamental interest in how the virus’s chromosomes might look and function and led to unexpected discoveries of how the viral infection is established in human cells.”
Dr. Yael David, chemical biologist at MSK
Study first author Dr. Nicholas Prescott, pursued the research in the David Lab as his graduate thesis. “This is a