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Virology. 2015 May;479-480:672-86. doi: 10.1016/j.virol.2015.02.031. Epub 2015 Mar 7.

Molecular biology of hepatitis B virus infection.

Author information

1
Fox Chase Cancer Center, Philadelphia, PA 19111, USA. Electronic address: Christoph.Seeger@fccc.edu.
2
Fox Chase Cancer Center, Philadelphia, PA 19111, USA.

Abstract

Human hepatitis B virus (HBV) is the prototype of a family of small DNA viruses that productively infect hepatocytes, the major cell of the liver, and replicate by reverse transcription of a terminally redundant viral RNA, the pregenome. Upon infection, the circular, partially double-stranded virion DNA is converted in the nucleus to a covalently closed circular DNA (cccDNA) that assembles into a minichromosome, the template for viral mRNA synthesis. Infection of hepatocytes is non-cytopathic. Infection of the liver may be either transient (<6 months) or chronic and lifelong, depending on the ability of the host immune response to clear the infection. Chronic infections can cause immune-mediated liver damage progressing to cirrhosis and hepatocellular carcinoma (HCC). The mechanisms of carcinogenesis are unclear. Antiviral therapies with nucleoside analog inhibitors of viral DNA synthesis delay sequelae, but cannot cure HBV infections due to the persistence of cccDNA in hepatocytes.

KEYWORDS:

Hepatitis B virus; Pathogenesis; Replication

PMID:
25759099
PMCID:
PMC4424072
DOI:
10.1016/j.virol.2015.02.031
[Indexed for MEDLINE]
Free PMC Article

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