Researchers from Duke and UNC team up to find an answer, with funding from the two institutions’ NIH Clinical and Translational Science Awards (CTSA).
For hundreds of millions of people around the world with chronic hepatitis B infection, anti-viral treatments do a good job of keeping the virus under wraps. Anti-viral treatments are essential in slowing damage to the liver, reducing the chance of liver cancer, and helping people live longer. But in the vast majority of cases, there is no end to the infection. If a patient stops medication for any reason, the hepatitis B virus (HBV) re-emerges. The cause of its resilience is circular bits of DNA, called covalently closed circular DNA, or cccDNA, that lurk in the liver cells of infected patients.
“Treatment blocks new viral replication,” said Lishan Su, a professor of microbiology and immunology at the University of North Carolina, Chapel Hill. “It doesn’t touch this cDNA.” When treatment stops, new virus is produced from these cccDNA templates, he continued. As a result, “you need almost lifetime (or very long-term) treatment.”