Hepatitis B virus (HBV) life cycle (HBV life cycle)

The Hepatitis B virus (HBV) life cycle is a complex multi-step process that begins with the virus binding to the sodium taurocholate cotransporting polypeptide (NTCP) receptor on the surface of hepatocytes (Yan et al., 2012, eLife). Following entry and uncoating, the viral relaxed circular DNA (rcDNA) is transported to the nucleus where it is repaired into covalently closed circular DNA (cccDNA), which serves as a stable transcriptional template for all viral RNAs (Nassal, 2015, Gut). These transcripts include pregenomic RNA (pgRNA), which is encapsulated and reverse-transcribed by the viral polymerase into new DNA genomes (Seeger & Mason, 2015, Microbiology Spectrum). Chronic HBV infection is a major driver of global liver disease, frequently progressing to cirrhosis and hepatocellular carcinoma (HCC) (Tang et al., 2018, JAMA). Current therapeutic interventions primarily utilize nucleos(t)ide analogues like Tenofovir and Entecavir to inhibit the viral polymerase, effectively suppressing DNA replication but failing to eliminate the cccDNA reservoir (European Association for the Study of the Liver, 2017, Journal of Hepatology). Consequently, lifelong treatment is often required, and research is now focused on novel targets within the life cycle, such as entry inhibitors (e.g., Bulevirtide) and capsid assembly modulators, to achieve a functional cure (Yuen et al., 2019, The Lancet).

Other names

HBV replication cycleHepatitis B viral replicationHBV infection cycle

Inhibition of viral reverse transcriptase, entry inhibition, capsid assembly modulation, and immune stimulation.