ArticleJournal of virology1999
The mechanism of an immature secretion phenotype of a highly frequent naturally occurring missense mutation at codon 97 of human hepatitis B virus core antigen.
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 74 papers.
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Who cites it
74 citing papers in PubMed, 111 citations in OpenAlex.
- Cryo-EM structures of HBV capsids from human cells at near-atomic resolution.Structure (London, England : 1993) · 2026Article
- The HBV variant CpF97L supports the secretion of pgRNA-containing virions at a level much greater than WT HBV.Journal of virology · 2025Article
- Induction of hepatitis B core protein aggregation targeting an unconventional binding site.eLife · 2025Article
- Pharmacomodulation of a ligand targeting the HBV capsid hydrophobic pocket.Chemical science · 2022Article
- Hepatitis B virus virion secretion is a CRM1-spike-mediated late event.Journal of biomedical science · 2022Article
- A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion.Journal of biomedical science · 2021Article
- The Hepatitis B Virus Nucleocapsid-Dynamic Compartment for Infectious Virus Production and New Antiviral Target.Biomedicines · 2021Review
- Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97.Viruses · 2021Article
- Conformational Plasticity of Hepatitis B Core Protein Spikes Promotes Peptide Binding Independent of the Secretion Phenotype.Microorganisms · 2021Article
- A pocket-factor-triggered conformational switch in the hepatitis B virus capsid.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Review
- The Integrity of the Intradimer Interface of the Hepatitis B Virus Capsid Protein Dimer Regulates Capsid Self-Assembly.ACS chemical biology · 2020Article
- Targeting the multifunctional HBV core protein as a potential cure for chronic hepatitis B.Antiviral research · 2020Review
- Hepatitis B Virus DNA is a Substrate for the cGAS/STING Pathway but is not Sensed in Infected Hepatocytes.Viruses · 2020Article
- Mutations and methods of analysis of mutations in Hepatitis B virus.AIMS microbiology · 2020Review
- Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model.Journal of virology · 2019Article
- Direct interaction between the hepatitis B virus core and envelope proteins analyzed in a cellular context.Scientific reports · 2019Article
- Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate.Antiviral research · 2019Article
- Hepatitis B virus core protein phosphorylation: Identification of the SRPK1 target sites and impact of their occupancy on RNA binding and capsid structure.PLoS pathogens · 2018Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A very frequent missense mutation at codon 97 of human hepatitis B virus (HBV) core antigen (HBcAg) has been found in chronic carriers worldwide. Functional characterization of this mutant revealed one intracellular and two extracellular phenotypes in contrast to wild-type HBV: (i) a 6- to 12-fold decrease in the level of the full-length relaxed circular DNA, a 4- to 5-fold decrease in the plus-strand DNA, and an approximately 1.8-fold decrease in the minus-strand and overall DNA levels in the intracellular viral core particles; (ii) a 5.7-fold increase in the immature secretion of Dane particles, containing minus-strand, single-stranded virion DNA; and (iii) a significant reduction of nonenveloped core particles in the medium. The steady-state levels of mutant and wild-type core proteins expressed from the same vector appeared to be similar. Using a complementation assay and gradient centrifugation analysis, we demonstrated that this mutant core protein alone is necessary and sufficient for immature secretion. The decreased level of intracellular HBV DNA is caused by both the cis defect of the mutant genome and the trans defect of the mutant core protein. We have dissected further the relationship between the intracellular and extracellular phenotypes of mutant F97L. The pleiotropic effects of the HBcAg codon 97 mutation were observed consistently in several different experimental settings. The mechanism and biological significance of these findings are discussed.
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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.