Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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.

Journal of virology - 1 Jul 1999

Yuan T T, Sahu G K, Whitehead W E, Greenberg R, Shih C

Abstract excerpt

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-fol...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Codon
Share to DNA, Single-Stranded
Share to Hepatitis B Core Antigens

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hepatitis B Surface Antigens

Share to Hepatitis B virus

Share to Immunoblotting

Share to Virion

Share to Virus Assembly

Source

Open in PubMed Open full text

Identifiers

PMID: 10364324
DOI: 10.1128/JVI.73.7.5731-5740.1999
PMCID: PMC112633

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-10364324-2026-09-04.1. Manifest publication-graph-cohort-2026-09-04.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

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.PMID 10364324Read ↗

Subtype-independent immature secretion and subtype-dependent replication deficiency of a highly frequent, naturally occurring mutation of human hepatitis B virus core antigen.Semantic proximity Read ↗

A frequent, naturally occurring mutation (P130T) of human hepatitis B virus core antigen is compensatory for immature secretion phenotype of another frequent variant (I97L).Semantic proximity Read ↗

A cis/trans genetic test for pleiotropic phenotypes associated with a frequent naturally occurring mutation at amino acid 97 of HBV core protein.Semantic proximity Read ↗

Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion.Semantic proximity Read ↗

Functional characterization of naturally occurring variants of human hepatitis B virus containing the core internal deletion mutation.Semantic proximity Read ↗

Virion Secretion of Hepatitis B Virus Naturally Occurring Core Antigen Variants.Semantic proximity Read ↗

Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus.Semantic proximity Read ↗

Low-level secretion of human hepatitis B virus virions caused by two independent, naturally occurring mutations (P5T and L60V) in the capsid protein.Semantic proximity Read ↗

Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus.Semantic proximity Read ↗

Nucleolar Localization of Human Hepatitis B Virus Capsid ProteinSemantic proximity Read ↗

Naturally occurring mutations define a novel function of the hepatitis B virus core promoter in core protein expression.Semantic proximity Read ↗

Dual defects in HBsAg antigenicity and secretion caused by the C138R mutation in the S gene trigger occult hepatitis B virus infection.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.