Molecular Biology of Hepatitis B Virus Infection
By C. Seeger, W. Mason. Virology, 2015
791 citations recorded by the source corpus.
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 life long, 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.
Subfields: Epidemiology, Hepatology
View Paper: https://www.semanticscholar.org/paper/a372e31050ce9762e4104109236753e12bfde6b5
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Citations in the corpus
- EASL 2017 Clinical Practice Guidelines on the management of hepatitis B virus infection. (2017, background): “2 kb), partially double-stranded, relaxedcircular (rc) DNA features 4 open reading frames encoding 7 proteins: HBeAg (HBV e antigen, secreted dimeric protein), HBcAg (HBV core antigen, viral capsid protein), HBV Pol/RT (polymerase, reverse transcriptase activity), PreS1/PreS2/HBsAg (large, medium, a”