Discovering the mechanisms underlying HBV persistence in chronic liver disease

Inside a single liver cell, oxygen levels may determine whether the hepatitis B virus (HBV) can establish a long-term infection. This matters because chronic hepatitis B affects hundreds of millions of people worldwide. Current drugs suppress the virus but rarely eliminate it, leaving patients at risk of progressive liver disease, including cirrhosis and cancer. The virus persists because its DNA genome remains inside liver cells, and the immune system fails to clear it. The researchers have shown that oxygen concentration influences how readily HBV replicates, suggesting that low-oxygen conditions—common in diseased liver tissue—may shield the virus from both immune attack and drug action. If the hypothesis holds, this work could reveal why HBV infection varies so dramatically between different regions of the same liver and between different phases of disease. The team has developed a technique to visualise individual viral RNA molecules inside intact liver tissue, combined with spatial transcriptomics to map immune activity around infected cells. This is fundamental science: it aims to uncover a core biological mechanism that has been invisible in standard population-level studies. A deeper understanding of how oxygen and local immune control interact could eventually point toward therapies that make liver cells less hospitable to the virus, rather than just suppressing its replication.