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HBV Integration Oncogenesis — SCE Infectious Diseases MCQ

Instant feedback + full explanation. One question, done properly.

HardHepatitisHBV Integration OncogenesisSCE Infectious Diseases

A 50-year-old man with chronic hepatitis B on Entecavir develops hepatocellular carcinoma despite 5 years of viral suppression (HBV DNA undetectable). He asks why he developed cancer despite treatment. What is the explanation?

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Reveal the answer and explanation

Correct answer: A — HBV DNA integrates into the host hepatocyte genome early in infection — integrated HBV sequences can drive oncogenesis independently of viral replication; NUCs suppress replication but cannot eliminate integrated DNA

HBV DNA integration into the host genome occurs very early after infection (within days). These integrated sequences — particularly those containing the HBx gene and truncated preS/S sequences — can drive hepatocarcinogenesis through insertional mutagenesis, chromosomal instability, and epigenetic changes. NUC therapy suppresses viral replication (cccDNA → pgRNA → new virions) but cannot eliminate already-integrated HBV DNA. This is why HCC risk persists even with sustained viral suppression, particularly in patients with established cirrhosis.

Reference: EASL 2024 – HBV and HCC; NICE CG165; Lancet Gastro 2022 – HBV integration