Association of hepatitis B virus genomes with active chromatin hubs challenges host replication fidelity, leading to DNA damage.

ABSTRACT: Hepatitis B virus (HBV), the leading cause of liver cancer, infects almost 300 million individuals worldwide. Although HBV-infected patients benefit from drug regimens that help control chronic infection, they are rarely clinically cured of HBV. The HBV genome persists in the nucleus of infected hepatocytes as a covalently closed circular DNA (cccDNA) molecule, a reservoir of HBV DNA molecules that serves as the template for reactivation of long-term chronic HBV. Despite playing a central role in the viral life cycle, little is understood about where cccDNA molecules localize, why they are so stable, and how they impact the host nuclear compartment. Here, we show that HBV genomes in cell line models provoke cellular replication stress early in infection, which culminates in global DNA dama

SUBMITTER: Marcoe GJ 

PROVIDER: S-EPMC12646004 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature