ArticleJournal of virology2000
Low-level secretion of human hepatitis B virus virions caused by two independent, naturally occurring mutations (P5T and L60V) in the capsid protein.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 81 citations in OpenAlex.
- Antiviral Activity and Pharmacokinetics of the Hepatitis B Virus (HBV) Capsid Assembly Modulator GLS4 in Patients With Chronic HBV Infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Trial
- Induction of hepatitis B core protein aggregation targeting an unconventional binding site.eLife · 2025Article
- HBc: the multifunctional architect of HBV replication, immune evasion, and therapeutic innovation.Frontiers in immunology · 2025Review
- Pharmacomodulation of a ligand targeting the HBV capsid hydrophobic pocket.Chemical science · 2022Article
- Constrained evolution of overlapping genes in viral host adaptation: Acquisition of glycosylation motifs in hepadnaviral precore/core genes.PLoS pathogens · 2022Article
- Hepatitis B virus virion secretion is a CRM1-spike-mediated late event.Journal of biomedical science · 2022Article
- Molecular characteristics of the full-length genome of occult hepatitis B virus from blood donors in China.Scientific reports · 2022Article
- 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
- Review
- Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model.Journal of virology · 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
- Common and Distinct Capsid and Surface Protein Requirements for Secretion of Complete and Genome-Free Hepatitis B Virions.Journal of virology · 2018Article
- Hepatitis B virus core antigen mutations predict post-operative prognosis of patients with primary hepatocellular carcinoma.The Journal of general virology · 2017Article
- Characterization of the disassembly and reassembly of the HBV glycoprotein surface antigen, a pliable nanoparticle vaccine platform.Virology · 2017Article
- The Structural Biology of Hepatitis B Virus: Form and Function.Annual review of virology · 2016Review
- Assembly and Release of Hepatitis B Virus.Cold Spring Harbor perspectives in medicine · 2015Review
- Core protein: A pleiotropic keystone in the HBV lifecycle.Antiviral research · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The functional significance of naturally occurring variants of human hepatitis B virus (HBV) remains largely unknown. Previously, we reported an immature secretion phenotype caused by a highly frequent mutation at amino acid 97 of the HBV core (capsid) protein (HBcAg). This phenotype is characterized by a nonselective and excessive secretion of virions containing an immature genome of single-stranded viral DNA. To extend our study of virion secretion to other naturally occurring variants, we have characterized mutations at HBcAg codons 5, 38, and 60 via site-directed mutagenesis. Although the phenotype of the mutation at codon 38 is nearly identical to that for the wild-type virus, our study reveals that a single mutation at codon 5 or 60 exhibits a new extracellular phenotype with significantly reduced virion secretion yet maintains normal intracellular viral DNA replication. A complementation study indicates that the mutant core protein alone is sufficient for the "low-secretion" phenotype. Furthermore, the low-secretion phenotype of the codon 5 mutant appears to be induced by the loss of a parental proline residue, rather than by the gain of a new amino acid. Our study underscores the core protein as another crucial determinant in virion secretion, in addition to the known envelope proteins. Our present results suggest that a very precise structure of both alpha-helical and nonhelical loop regions of the entire HBcAg molecule is important for virion secretion. The low-secretion variants may contribute to the phenomenon of gradually decreasing viremia in chronic carriers during the late phase of persistent infection.
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Registered trials
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.