title: Hepadnavirus envelope proteins regulate covalently closed circular DNA amplification.
abstract: Primary duck hepatocytes were infected with a mutant duck hepatitis B virus defective in envelope protein but competent for viral DNA synthesis. Cells infected by this mutant accumulated higher levels of viral covalently closed, circular DNA (cccDNA) than those infected by wild-type virus. The accumulation of high levels of cccDNA was due to a failure of the mutant-infected cells to suppress de novo cccDNA synthesis compared with suppression by cells infected by the wild type. The envelope-defective virus failed to establish a persistent infection in vitro, possibly because of a virus-mediated cell death. Therefore, one or both viral envelope proteins are required for regulation of cccDNA synthesis and for maintenance of persistent infection in vitro.
authors.affiliation: Department of Cell Biology, University of New Mexico School of Medicine, Albuquerque 87131.
authors.forename: J
authors.initials: J
authors.lastname: Summers
authors.forename: P M
authors.initials: PM
authors.lastname: Smith
authors.forename: A L
authors.initials: AL
authors.lastname: Horwich
mesh_terms: D000818:Animals; D002460:Cell Line; D002478:Cells, Cultured; D004270:DNA, Circular / Q000235:genetics*; D004279:DNA, Viral / Q000235:genetics / Q000302:isolation & purification; D004372:Ducks; D005784:Gene Amplification; D015967:Gene Expression Regulation, Viral; D005814:Genes, Viral; D015613:Hepadnaviridae / Q000235:genetics*; D008099:Liver / Q000378:metabolism / Q000382:microbiology; D009154:Mutation; D010957:Plasmids; D014162:Transfection; D014759:Viral Envelope Proteins / Q000378:metabolism*
chemical_list: D004270:DNA, Circular; D004279:DNA, Viral; D014759:Viral Envelope Proteins