H — Hepatitis B Virus (HBV)
HBV is a small, enveloped DNA virus in the family Hepadnaviridae. Its partially double-stranded relaxed circular DNA genome is converted in the nucleus into covalently closed circular DNA (cccDNA), which serves as a stable transcriptional template. Viral replication involves reverse transcription of a pregenomic RNA intermediate within nucleocapsids.
HBV is noncytopathic; liver injury is primarily immune-mediated. Cytotoxic T lymphocytes recognize HBV-infected hepatocytes, producing both viral clearance and hepatocellular damage. In perinatally infected individuals, immune tolerance may allow prolonged high-level replication with minimal early inflammation.
Chronic HBV infection can progress through phases characterized by HBeAg status, viral load, and ALT levels. Persistent inflammation promotes fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Oncogenesis involves chronic inflammation, integration of HBV DNA into the host genome, and expression of oncogenic viral proteins such as HBx.
Current therapies (nucleos(t)ide analogues) suppress viral replication but do not eliminate cccDNA. Research efforts focus on functional cure strategies, including immune modulation, cccDNA targeting, and therapeutic vaccines.
HBV is a small, enveloped DNA virus in the family Hepadnaviridae. Its partially double-stranded relaxed circular DNA genome is converted in the nucleus into covalently closed circular DNA (cccDNA), which serves as a stable transcriptional template. Viral replication involves reverse transcription of a pregenomic RNA intermediate within nucleocapsids.
HBV is noncytopathic; liver injury is primarily immune-mediated. Cytotoxic T lymphocytes recognize HBV-infected hepatocytes, producing both viral clearance and hepatocellular damage. In perinatally infected individuals, immune tolerance may allow prolonged high-level replication with minimal early inflammation.
Chronic HBV infection can progress through phases characterized by HBeAg status, viral load, and ALT levels. Persistent inflammation promotes fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Oncogenesis involves chronic inflammation, integration of HBV DNA into the host genome, and expression of oncogenic viral proteins such as HBx.
Current therapies (nucleos(t)ide analogues) suppress viral replication but do not eliminate cccDNA. Research efforts focus on functional cure strategies, including immune modulation, cccDNA targeting, and therapeutic vaccines.