ArticleJournal of virology1999
Extensive mutagenesis of the hepatitis B virus core gene and mapping of mutations that allow capsid formation.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed.
- Induction of hepatitis B core protein aggregation targeting an unconventional binding site.eLife · 2025Article
- GE11-antigen-loaded hepatitis B virus core antigen virus-like particles efficiently bind to TNBC tumor.Frontiers in oncology · 2023Article
- The Integrity of the Intradimer Interface of the Hepatitis B Virus Capsid Protein Dimer Regulates Capsid Self-Assembly.ACS chemical biology · 2020Article
- Intracellular Trafficking of HBV Particles.Cells · 2020Review
- Review
- Direct interaction between the hepatitis B virus core and envelope proteins analyzed in a cellular context.Scientific reports · 2019Article
- Enhanced stability of a chimeric hepatitis B core antigen virus-like-particle (HBcAg-VLP) by a C-terminal linker-hexahistidine-peptide.Journal of nanobiotechnology · 2018Article
- Host factors involved in hepatitis B virus maturation, assembly, and egress.Medical microbiology and immunology · 2012Review
- Naturally occurring core immune-escape and carboxy-terminal mutations\truncations in patients with e antigen negative chronic hepatitis B.Hepatology international · 2012Article
- Characterization of the pleiotropic effects of the genotype G-specific 36-nucleotide insertion in the context of other hepatitis B virus genotypes.Journal of virology · 2011Article
- Hepatitis B Virus Genotype G forms core-like particles with unique structural properties.Journal of viral hepatitis · 2011Article
- A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly.Biochemistry · 2009Article
- Comparison of serum humoral responses induced by oral immunization with the hepatitis B virus core antigen and the cholera toxin B subunit.Clinical and vaccine immunology : CVI · 2008Article
- A structural model for duck hepatitis B virus core protein derived by extensive mutagenesis.Journal of virology · 2007Article
- Hepatitis B virus morphogenesis.World journal of gastroenterology · 2007Review
- Phosphorylation of hepatitis B virus Cp at Ser87 facilitates core assembly.The Biochemical journal · 2006Article
- The 113th and 117th charged amino acids in the 5th alpha-helix of the HBV core protein are necessary for pgRNA encapsidation.Virus genes · 2003Article
- Mapping of amino acid side chains on the surface of hepatitis B virus capsids required for envelopment and virion formation.Journal of virology · 2003Article
- Hepatitis B virus core gene mutations which block nucleocapsid envelopment.Journal of virology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We generated a large number of mutations in the hepatitis B virus (HBV) core gene inserted into a bacterial expression vector. The new mutagenesis procedure generated deletions and insertions (as sequence repeats) of various lengths at random positions between M1 and E145 but not substitutions. The R-rich 30-amino-acid C-terminal domain was not analyzed. A total of 50,000 colonies were tested with a polyclonal human serum for the expression of hepatitis B core or e antigen. A total of 110 mutants randomly chosen from 1,500 positive colonies were genotyped. Deletions and insertions were clustered in four regions: D2 to E14, corresponding to the N-terminal loop in a model for the core protein fold (B. Bottcher, S. A. Wynne, and R. A. Crowther, Nature 386:88-91, 1997); V27 to P50 (second loop); L60 to V86 (upper half of the alpha helix forming the N-terminal part of the spike and the tip of the spike); and V124 to L140 (C-terminal part of the C-terminal helix and downstream loop). Deletions or insertions in the remaining parts of the molecule forming the compact center of the fold seemed to destabilize the protein. Of the 110 mutations, 38 allowed capsid formation in Escherichia coli. They mapped exclusively to nonhelical regions of the proposed fold. The mutations form a basis for subsequent analysis of further functions of the HBV core protein in the viral life cycle.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.